sensory systems flashcards
(499 cards)
1
Q
What is the role of the premotor cortex?
A
Coordinates voluntary movements
2
Q
What is the role of the primary motor cortex?
A
Voluntary movement.
3
Q
What is the role of the primary somatosensory cortex?
A
Somesthetic sensations and proprioception.
4
Q
What is the role of the sensory association areas?
A
Integration of sensory information.
5
Q
What is the role of the visual association areas?
A
higher vision processing.
6
Q
What is the role of the primary visual cortex?
A
Vision
7
Q
What is the role of Wernicke’s area?
A
Language comprehension
8
Q
What is the role of the primary auditory cortex?
A
Hearing.
9
Q
What is the role of the Limbic association cortex?
A
emotions, learning and memory.
10
Q
What is the role of the olfactory cortex?
A
Smell.
11
Q
What is the role of Broca’s area?
A
speech formation
12
Q
What is the role of the prefrontal association areas?
A
idea and plan for voluntary movement, thoughts, personality.
13
Q
What is the function of sensory systems?
A
Sense nature of the internal and external environment.
14
Q
What is in charge of the sensors of the internal environment?
A
The vagus nerve.
15
Q
What is somatosensation?
A
The physiological process by which neural substrates are activated by physical stimuli resulting in the perception of what we describe as touch, pressure, pain, etc.
16
Q
What is the sensation of the environment called?
A
Somatosensation
17
Q
What is proprioception?
A
The sense of limb/body position and movement.
18
Q
What is a sensory receptor?
A
A specialised excitable cell sensitive to a form of physical energy (modality)
19
Q
What are the 4 modalities of sensory receptors?
A
Mechanical, Thermal, Chemical, Electromagnetic.
20
Q
What are the 4 types of receptor (think modality).
A
Mechanoreceptor, Thermoreceptor, Chemoreceptor, Photoreceptor.
21
Q
What is the law of specific nerve energies?
A
Receptors are (usually) specific to a particular modality.
22
Q
What is meant by adequate stimulus in reference to receptor specificity?
A
The modality to which a receptor responds best.
23
Q
What do photoreceptors sense?
A
Photons of light
24
Q
What do chemoreceptors for taste sense?
A
Chemicals dissolved in saliva.
25
What do chemoreceptors for smell sense?
Chemicals dissolved in mucus.
26
What do chemoreceptors for pain sense?
Chemicals in extracellular fluid
27
What do chemoreceptors for blood oxygen sense?
Oxygen dissolved in plasma.
28
What do chemoreceptors for blood pH sense?
Free hydrogen ions in the plasma.
29
What do thermoreceptors for warmth detect?
increase in temperatures between 30-43 degrees.
30
What do thermoreceptors for cold detect?
Decrease in temperatures between 35-20 degrees.
31
What are the 3 main types of mechanoreceptors?
Baroreceptors, Osmoreceptors, Hair cells.
32
What do baroreceptors sense and detect?
Blood pressure by measuring the stretch of specific blood vessels walls.
33
What do osmoreceptors sense and detect?
Osmolarity of extracellular fluid by the swelling (stretch) of the receptor cells.
34
What are the two things that hair cells sense and how do they detect them?
Sound - sound waves
Balance and equilibrium - acceleration.
35
What are the main components of neuronal structure?
Cell body (soma)Neurites:- dendrites- axons - synapses
36
What is a neurite?
any type of process or protrusion extending out from the cell body of a neuron
37
What is transduction?
Conversion of physical energy to a receptor potential in the receptor neuron.
38
What are the 5 types of receptors in the skin?
Meissner corpuscle, Pacinian corpuscle, Ruffini's corpuscles, Merkel's disks, Free nerve endings.
39
What is difference between the stimulus and the resulting receptor potentials?
Stimulus is a flat on/off, receptor potentials are graded potentials (gentle slope down through duration of the stimulus)
40
How do anaesthetics work?
They block the ion channels in the mechanoreceptors so that transduction cannot take place.
41
What are the two main types of transduction?
One in which the cells that receives also transduces and passes on the information (e.g. pacinian corpuscle).
One in which there are two cells (think receptor cell which synapses an afferent neuron).
42
What is meant by afferent?
A neuron in the peripheral nervous system that conducts action potentials to the central nervous system
43
What is meant by sensory coding?
Representation of stimulus in terms of action potentials.(e.g. small stimulus less frequent firing, larger = more firing)
44
Give an example of both single and two cell transduction.
Single = pacinian corpuscle
Two = hair cell in cochlea.
45
Briefly outline how cochlea hair cells receive and transduce information.
The vibrations in the cochlea fluid cause ion channels to open/close on the cochlear hair cells depending on the type of vibration.- Open, causes receptor potentials.- The auditory afferents then transduce to the nervous system.
46
What is a sensory unit?
Receptor with an afferent neuron.
47
Outline the sensory pathway from PNS to CNS
PNS:- stimulus- receptors- afferent (first order neuron)CNS:- Spinal cord/brainstem- second order neuron- Thalamus- Third order neuron- Cortex.
48
What does tonotopic organisation mean? (sound)
each sound frequency is represented in a narrow strip along the surface of the cortex in relation to its frequency.
49
Briefly outline how cochlear implants work.
A microphone protrudes from the side of the head, which is connected to electrodes that are implanted in the cochlea.These inserted electrodes will stimulate the different parts of the cochlea depending on the wavelengths picked up by the microphone, thereby transducing the information for the cochlea.
50
Briefly outline the somatosensory pathways (7).
1. Receptor
2. Afferent neuron
3. Spinal cord
4. Second order neuron
5. Thalamus
6. Third order neuron
7. Primary somatosensory cortex.
51
What is stereognosia?
Inability to identify objects by touch alone.
52
What is action defects?
Lacking fine motor skills.
53
What is the aim of the sensory systems?
To serve action.
54
What is the role of gustation?
To identify food and avoid noxious and toxic substances.
55
How many taste compounds can we recognise and give some examples.
Hundreds:- Free protons (H+ acid)- Complex organic compounds (sugars, amino acids)
56
How many dimensions of taste are there? What are they?
5Sweet, sour, bitter, salty, umami
57
What produces the sensation of umami? Give an example of a substance.
It's induced by glutamate.MSG (monosodium glutamate)
58
What are the three types of papillae and where are they located on the tongue?
Fungiform - found from the tip to 3/4 the way back, all over medial surface of the tongue.
Foliate - Found laterally at the back of the tongue.
Vallate - Found back middle in a V shape (point being furthest back)
59
What are the three types of taste cell?
Type I, Type II, Type III
60
What is unique about taste cells as a sensory unit?
They can regenerate (if they die they can be replaced/grow back)
61
What is the organisation of taste cells in a taste pore?
Type I - Thin and at the top, soma closer to the opening.
Type II- Large and soma sits in the middle.
Type III- Medium sized and soma sits closer to the body
62
What is the approximate number of taste cells per taste bud?
Roughly 100
63
Afferent projections of what type of nerves are found in taste buds?
Cranial nerves.
64
Provide a brief overview of how type II and III cells respond to stimulants in the taste bud.
The receptor cells respond to stimulants in the taste bud with graded changes in polarisation (and depolarisation) and neurotransmitter release.DO NOT SIGNAL DIRECTLY TO BRAIN
65
How is resting potential established in type II and III taste cells?
Sodium/potassium exchanger ensures high intracellular K+ and high extracellular Na+
Leakage K+ channels allow K+ to leave the cell, establishing potential (a positive charge outside the cell)
66
How does synaptic release occur in type II and III taste cells?
Voltage gated cation channels (Na+ and Ca2+) open, allowing Na+/Ca2+ back into cell reducing potential (more positive inside now).This causes neurotransmitter release into synaptic cleft and action potential transmitted.
67
What tastes do type II cells detect?
Nasty- bitter sensitive cellsNice - sweet and/or umami sensitive cells
68
What taste do type III cells detect?
Sour
69
What type of receptor are type II 'nasty' taste cells?
G protein coupled receptors. (Bitter)
70
Briefly outline the pathway of taste II receptors (think GPCR).
Ligand binds, changing confirmation.
G-alpha dissociates from beta/gamma subunits
Both these two different subunit clusters bind effector enzymes.
This starts a signalling cascade
This increases diffusible 'second messengers'(e.g. cAMP, cGMP, IP3)
71
Describe in detail the process of ligand binding to action potential in type II 'sweet' taste cells. (1)
Pair of GPCR's (Heterodimer) of T1R2 and T1R3.The ligand binds the extracellular cleft formed by the heterodimer.This change in conformation releases Gustducin (Gbetagamma)This interacts with PLC which catalyses PIP2 to IP3 and DAG.IP3 binds with its ligand gated Ca2+ channel (IP3 receptor).This catalyses stores of Ca2+ in the EPR, increasing intracellular calcium which binds to TRPM5.This allows the influx of calcium and causes depolarisation.
72
Describe in detail the process of ligand binding to depolarisation in type IIumami taste cells. (2)
mGluR1 (metabotropic glutamate receptor)The ligand binds the extracellular cleft.This change in conformation releases Gustducin (Gbetagamma)This interacts with PLC which catalyses PIP2 to IP3 and DAG.IP3 binds with its ligand gated Ca2+ channel (IP3 receptor).This catalyses stores of Ca2+ in the EPR, increasing intracellular calcium which binds to TRPM5.This allows the influx of calcium and causes depolarisation.
73
Describe in detail the process of ligand binding to depolarisation in type II 'nasty' bitter taste cells.
T2R GPCR.The ligand binds the extracellular cleft.This change in conformation releases Gustducin (Gbetagamma)This interacts with PLC which catalyses PIP2 to IP3 and DAG.IP3 binds with its ligand gated Ca2+ channel (IP3 receptor).This catalyses stores of Ca2+ in the EPR, increasing intracellular calcium which binds to TRPM5.This allows the influx of calcium and causes depolarisation.
74
How many types of T2R are there?
30 types
75
Outline how type III sour cells detect sour and the path to depolarisation.
First of all, Na+/K+ exchanger helps to maintain resting potential (K+ in, Na+ out).pH sensitive K+ leakage channel stops the channel from depolarising without stimuli.H+ channels allow H+ ions to enter.This means that when acid is present, acidification of the cell occurs. This causes the closing of the K+ leakage channels which will cause depolarisation as charge inside the cell rises.5HT (serotonin) transmits the signal.
76
Outline how type III salty cells detect salty and the path to depolarisation.
LESS KNOWN!ENaC channel (epithelial sodium channel).The presence of salt extracellularly increases the conc gradient, causing more Na+ to move into the cell.This causes depolarisation.Serotonin transmits this info.
77
What are T2Rs and what do they detect?
GPCRs and bitter compounds
78
Why are there so many T2Rs ?
GPCRs recognise ligands based upon match between ligand 3D shape and chemical characteristics.Therefore, as there are lots of bitter compounds, there needs to be lots of GPCRs to detect them
79
Outline the relationship between T2Rs and a single type II taste cell.
They typically express more than 1 type of T2R
80
What are isothiocyonates?
Bitter chemicals that are found in veg.
81
What is PTC (phenylthiocarbamide)? What is interesting about it?
An analog of isothiocynates which are also bitter.Some people taste bitter from exposure to it, some people don't.
82
What difference is evident between bitter and non bitter tasters of PTC (phenylthiocarbamide)?
Incidence of iodine deficiency higher in non-tasters.
83
What did Kim et al (2003) find in their study into molecular genetics of PTC sensitivity?
Most variation in human population was caused by polymorphisms at the TAS2R38 (bitter GPCR)
84
What did Wooding et al (2006) find in their study into molecular genetics of PTC sensitivity?
Variation in Chimps also arise in TAS2R38 polymorphism, but not in the same one as humans.
85
Outline the possible implications of the difference between the non-taster/taster TAS2R38 alleles.
PTC non-tasters don't lack TAS2R38, potentially it detects other bitter compounds which could lead to a heterozygote advantage (can detect more bitter compounds).
86
What can PTC teach us?
Bitterness is about avoiding toxins.Receptor affinity for different compounds is under strong selection.Changes in amino acid sequence of the receptor alter the compound it detects.Having a wide range of T2Rs allows a wide variety of toxins to be detected.
87
What shows that there is a fine tuning of receptor specificity by natural selection?
The varying levels of bitter taste threshold for quinine hydrochloride of various mammal feeding types (e.g., carnivore vs herbivore).
88
What does connections between neurons give an opportunity for?
Signal processing.
89
Outline the process from taste buds to the brain.
1.Taste bud receives information.
2.Its carried along the cranial nerves to the geniculate ganglion.
3.Then it passes through the nucleus of the solitary tract.
4.Up to the ventral posterior medial nucleus of the thalamus
5.Arrives in the gustatory cortex (anterior insula-frontal operculum)
90
What are the two options of how taste information is transmitted to the brain?
Option 1:Labelled line code
Option 2:Combinatorial code
91
What is meant by labelled line code?
Information is transmitted as separate information streams - each neuron at each stage responds to a single dimension of taste.
92
What is meant by combinatorial code?
Information is transmitted as a single merged stream - individual neurons respond to a combination of taste dimensions.
93
What prediction does labelled line code make in regards to gustation?
Each receptor cell should detect a single taste dimension and the perceived taste should be defined by the identity of receptor cell activated.Each postsynaptic neuron should receive input from receptor cells detecting the same dimension.
94
What are the problems of predicting gustatory information is transmitted using labelled line code?
Sweet and umami tastes can co-occur, therefore there must be some merging.Postsynaptic neurons are a combination of 'specialists' that respond to one taste and 'generalist' that respond to multiple tastes.
95
What conclusions can be made about the transmitting of information from taste cells to the brain?
Input to the brain is complex:- Gustatory neurons in cranial nerves have different degrees of preference to singular taste dimensions.- Some integration across dimensions at early stages.Combinatorial code:- taste discrimination occurs by the brain assessing activity across the population of neurons
96
Which three things influence your perception of flavour?
Gustation
Olfaction
Somatosensory
97
Name 3 things that influence our decision of what to eat.
Innate preferences
Learned associations
Satiety signals
98
Outline the two types of innate preferences that guide taste.
Innate aversions:- BitternessInnate cravings:- Sweet- Umami- Salty(which is determined by our NaCl balance)
99
Give an example of an association influencing taste.
Having shellfish on a boat and then being sea sick can lead to you disliking the shell fish.
100
Name three key features of taste conditioning.
Timing and number of pairings(can have up to an hour between)Longevity Stimulus generalisation
101
What does olfaction detect in land and aquatic animals?
Land: volatile hydrophobic compounds
Aquatic: Water soluble molecules
102
What are odorants?
Volatile, lipophylic organic compounds
103
Where does olfaction start?
The olfactory epithelium
104
Outline the structure of olfactory epithelium from nasal cavity out.
Cilia
Mucus
Dendrites(supporting cells around them)
Olfactory sensory neuron (soma)
Axons(basal cells around them)
Out to olfactory bulb.
105
Outline important information about olfactory sensory neurons.
They detect and signal to the brain - they don't synapse to an afferent neuron.They can regenerate throughout life.They fire action potentials in response to application of odorants.
106
What is the role of the lateral nasal gland?
A thermoregulatory gland that keeps the nasal cavity moist.
107
What is the importance of binding proteins in olfaction?
They are released so that they can grab odorants, presenting them for sensory neurons.
108
What is the environment of the lateral nasal gland?
aqueous mucus environment
109
Who are Linda Buck and Richard Axel and what is the importance of them?
They won the nobel prize in 1991 for finding 'A novel multigene family may encode odorant receptors: a molecular basis for odour recognition.
110
Which receptor class is vital for odorant detection?
GPCR
111
Outline the process of receptor ligand binding to action potential in olfaction.
GPCR.The odorant binds with the receptor protein.G-olf activates at binding
Separates into alpha and beta-gamma subunits
Free alpha subunit activates Adenylate Cyclase
This increases cAMPcAMP opens cation channels in membrane This allows positive charge to influx (Na+ and Ca2+)
Depolarisation, therefore AP.
112
What is the role of calcium in modulating olfaction in the receptor? (2 main overarching)
Calcium activates calcium gated chloride channels which causes Cl- efflux, therefore increasing the speed of depolarisation.Calcium activates calmodulin, which leads to activation of Phosphodiesterase E which deactivates adenylate cyclase- This stops cAMP production, effectively switching off the whole system more and more the longer a odorant is present (hence why a smell 'goes' if you're in it long enough)
113
Briefly outline the pathway from the first olfactory synapse to the specific areas of the brain olfactory information goes.
Olfactory bulbOlfactory nerve Olfactory tractOlfactory cortex (paleocortex)- Hippocampus- Amygdala- Hypothalamus- Thalamus--- Frontal cortex
114
Which parts of olfaction are processed in the following areas of the brain?- Hippocampus- Amygdala- Hypothalamus- Thalamus/Frontal cortex
- Hippocampus: odorants activating memory
- Amygdala: Emotion
- Hypothalamus: Feeding behaviours
- Thalamus/Frontal cortex: perception of the smell
115
What is special about the olfactory bulb in the mouse brain?
It's a proportionally large part of the brain (shows emphasis of smell in their perception).
116
Outline important information about odorants.
Thy are volatile compounds that are structurally distinct.They are individual elements that combine to create and odour - complex.
117
Outline humans detection and discrimination of odorants.
Detect hundreds of thousands of distinct odorants.Discriminate a few thousand odorants.
118
Outline the relevance of human gene number and how odorant receptor proteins work.
Human genome has around 20k genes.This means that we can't have a specific GPCR per odorant we detect - therefore each odorant receptor protein must recognise >1 odorant.
119
Outline the relationship between receptors and how they detect odorants.
Each receptor detects multiple odorants.Most odorants excite several receptors - dependent on concentration (e.g. perfume)- some odorants act as antagonists (combinations can antagonise)
120
Summarise the key information about how receptors and odorants interact for olfaction.(6 points)
Odorants bound by odorant receptors according to 3D structureEach receptor protein responds to several odorantsA huge number of odorants will be bound by one or more of these receptorsA smaller (but still v large) number of odorants will have a unique receptor activation profileComplex odours contain numerous odorants … almost infinite variety in receptor activation profilesConclusion: 1k olfactory receptor genes provide HUGE discriminatory power for odours
121
Outline the study into transgenic Lac-Z reporter mice.
SET-UP:Mice were taken and genetically modified in their olfactory receptor protein genes with Lac-Z.Lac-Z encodes b-galactosidase which metabolises X-gal to form a blue pigment.Native locus:promotor - coding sequenceGenetically modified locus - Lac-Z coding sequenceThis means that the receptor cells are labelled blue so we can see how they are expressed.RESULTS:The ~10k olfactory sensory neurons expressing a given olfactory receptor are distributed across the nasal epithelium.Their axons converge on just 2 specific locations (glomeruli) in the olfactory bulb. ~2k glomeruli in the olfactory bulb.WHAT THIS SHOWS:An odour is translated into:1.) a pattern of olfactory receptor activations, becomes 2.) a spatial pattern of activity in the olfactory bulb ‘Odour Map’
122
Outline what Lapil et al (2011) found out about olfaction.
Zones of olfactory epithelium respond to structurally similar compounds.Zones encode common perceptions
123
How is information about odours transmitted? (Type of code)
combinatorial code.
124
What are pheromones and what is their significance?
A pheromone is a secreted or excreted chemical factor that triggers a social response in members of the same species.
125
What is the name of the organ which detects pheromones? Outline the pathway to the brain of this information.
Vomeronasal organ.
Sensory neurons in the vomeronasal organ
Vomeronasal nerves
Accessory olfactory bulb
Hypothalamus- regulates the response due to pheromones.
126
Outline the receptor used in pheromone detection. How many families are there? What are their names and important information about them?
GPCR2 evolutionarily distinct families V1r (about 150 genes; v high interspecific variation; mostly pseudogenes in primates) V2r (about 100 genes)
127
Outline the process of receptor to depolarisation of pheromones.
Vomeronasal sensory neurons VR GPCR binds pheromoneG protein dissociatesG betagamma activates Phospholipase C (PLC)Catalyses PIP2 into IP3 and DAGDAG activates TRP2 cation channelsCations influxDEPOLARISATION :)
128
Briefly outline the behavioural effects of disrupting the vomeronasal system.
If a male mouse has a functional VNO it will respond to females by trying to mate and males by trying to fight.If you take a male mouse with a non-functional VNO (knockout TRP2 gene (no depolarisation can occur)) they will try mount a male castrated mouse covered in male piss.Shows that VNO and pheromones are important in social behaviour.
129
What is the eye?
Specialised photosensory organ.
130
What is a photoreceptor?
Cell specialised for light detection
131
What is a photopigment?
Protein + light absorbing cofactor.
132
Outline the important distinction about photopigments and their relationship to eyes and photoreceptors.
Many organisms have photopigments without having 'photoreceptors' or eyes.Even in animals:- not all photopigments are found in 'photoreceptors'- not all photoreceptors are found in eyes.
133
What is the role of the eye?
It's the optical apparatus to provide spatial resolution to photoreception.
134
Outline photoreceptors in Xenopus.
Dermal photoreceptors (melanophores) detect ambient light levels.They also adapt to light by pigments changing colour in response to light as a form of camouflage.
135
Outline a type of simple eyes and how they work.
Planarian eyes:- Eyes exist in pigmented pits which limit the range of directions from which light can reach each photoreceptor- By measuring photoactivity of different cells, they can detect where in the world is brighter.
136
What is -ve phototaxis? Give an example of an organism that uses it.
It is directed movement away from a source of light - planarian.
137
Briefly outline the structure of the compound eye of insects.
Are composed of thousands of units called ommatidia.
138
Outline the structure of ommatidia.
Have a crystalline cone and cornea which form a lens.They have photosensitive neurons/photoreceptors in a column.As light only enters from the front and it has pigmented cells which form a tube, this forms a fine collecting area.
139
What is meant by acuity in vision?
Capacity for seeing distinctly the details of an object.
140
Outline the acuity of the compound insect eye.
Medium acuity (closer objects = higher acuity)Each ommatidium = 1 pixel Therefore is limited to a few thousand
141
How do mirror eyes work? Give an example organism.
Scallop (has 60-100 small 1mm eyes)Light enters the eye through opening (pigment around to stop light coming through anywhere else), and bounces off of a concave mirror at the back which focuses the image onto an array of photoreceptors (like a reflective telescope).
142
How does the compound eye deal with distance?
Acuity is limited by the collecting area of the ommatidium - which increases with the distance from object.Simple inverse correlation between distance and acuity:- the further away the object is, the large space the collecting area covers, therefore lower acuity.
143
How does the mirror eye deal with distance?
The curvature of the mirror is designed so that the image is reflected onto a specific point.This means the focal length of the mirror is invariant (as it can't change its shape)Objects in focus at specific distances, but not at other.Acuity strongly depends on viewing distance.
144
Outline the lens eye.
It has a very high acuity.Cornea refracts 80%, lens variably refracts the other 20%.This means light can be focused on the retina at varying distances.In theory, each photoreceptor receives light from a different visual space (lots of pixels).
145
Which types of animals have the lens eye?
All vertebratesSome invertebrates:- Squid/Octopus- SpiderCertain types of jellyfish.
146
Outline refraction in reference to the eye.
Focusing divergent rays from a point in visual space into a single point on the retinal surface.
147
What controls the changing size of the lens?
The ciliary muscle/body.
148
Outline the process of refraction in the lens eye at long distances.
Light rays are near parallel so require little refraction to focus.Therefore lens is thin and needs low refractive power.Actions taken to make this occur:- Ciliary muscles relaxed- Suspensory ligaments taught- Lens pulled thin.Therefore refracts distant objects to back of retina.
149
Outline the process of refraction in the lens eye at short distances.
Light rays are still diverging so require greater refraction to focus.Therefore lens is thick and needs high refractive power.Actions taken to make this occur:- Ciliary muscles contracted- Suspensory ligaments loose- Lens small and thick.
150
What does accommodation mean in the eye?
Changing vision from distant to close:- Ciliary muscles contract- Lens thickens and refractive power increases- Pupils constrict.
151
What causes refractive errors?
They arise from problems with corneal or lens refraction.The distance from cornea to retina can be impacted by genes or experience.
152
What is myopia and how is it resolved?
Short sightedness.Eyes too deep/long and/or the refractive power of the cornea is too great.Near objects, reduction in accommodative change in lens can compensate.Diverging (concave) lens corrects
153
What is hyperopia and how is it resolved?
Long sightedness.Eyes too shallow/short and/or the refractive power of the cornea is too small.Far objects, accommodative change in the lens can compensate.Converging (convex) lens corrects
154
How many Opsin proteins are there per rod cell?
10^8
155
What are opsins?
Proteins that bind to light-reactive chemicals to underlie vision, phototaxis, circadian rhythms, and other light-mediated responses of organisms
156
What is retinal/retinaldehyde and what is its significance?
Retinaldehyde (which is a vitamin A derivative) is a polyene chromophore. Retinal, bound to proteins called opsins, is the chemical basis of visual phototransduction, the light-detection stage of visual perception.
157
What is a chromophore?
The factor of an opsin photopigment that absorbs light.
158
What are the two main types of retinaldehyde and what is the difference between them? What is their relationship?
11-cis retinaldehyde- has an important kink in the carbon chain
all-trans retinaldehyde- has no kink in carbon, linear version
11-cis retinaldehyde is activated into all-trans retinaldehyde due to light
They're both derivatives of Beta-carotene (vitamin A)
159
Outline the structure and functions of opsin proteins.
7 transmembrane domain G protein coupled receptor.Binds retinaldehyde.Functions:- translate isomerisation of retinaldehyde into a 'biological' signal- determines which wavelengths the retinaldehyde absorbs
160
Outline the relationship between 11-cis retinaldehyde, 11-all trans retinaldehyde and GPCRs.
11-cis retinaldehyde is a inverse agonist - strongly inhibits the GPCR11-all trans retinaldehyde activates the GPCR (occurs when light hits 11-cis retinaldehyde)
161
Outline the phototransduction cascade.
Retinaldehyde absorbs lightChanges opsin from inactive to active formActivated opsin binds to transducin (g-protein)Breaks into alpha subunit and beta-gamma subunitAlpha subunit binds to cGMP phosphodiesteraseLeads to reduction of cGMP activationLeads to closure of cGMP gated cation channels (cGMP opens cation channels, so long as there is lots of cGMP the cation channels stay open)
162
Outline how a single photon of light can have an impact in the phototransduction cascade.
Single photon of light can have a large effect.Activation of a single rhodopsin leads to activation of lots of transducin, which can lead to activation of lots of cGMP phosphodiesterase, in turn leading to reduction of activity of cGMP.
163
Outline how photoreceptors act in the dark.
Gated cation channels are open so ions rush in.Sodium potassium exchanger is in effect, increases the internal conc of potassium (whilst there is potassium leakage) and decreases internal Na+Overall this leads to depolarisation.Photoreceptors are excited and release glutamate in the dark.
164
What is the difference between rod and cone cells?
Rods have a long out segment, capture more photons and have a larger signal amplification cascade (more sensitive).Cones adjust their sensitivity to be active under any light level.They are never saturated - so you can always see.Have a higher acuityProvide colour vision.Are located in the fovea.
165
Name the layers of the retina
Photoreceptor layerOuter plexiformInner nuclear layerInner plexiform layerRetinal Ganglion Cells
166
Outline the connections of the photoreceptor layer
Makes connections with second order neurons in outer plexiform layer
167
Outline the connections of the outer plexiform layer.
Photoreceptor layer and inner nuclear layer makes connections here.No cell bodies here, just connections.
168
Outline the connections of the inner nuclear layer.
Makes connections with the outer plexiform layer
169
Outline the connections of the Inner plexiform layer.
No cell bodies, make connections with retinal ganglion cells in ganglion cell layer.
170
Outline what is special about retinal ganglion cells.
Are the only cells in the retina with axons, and the only cells in the retina that can form APs.
171
Outline the role of retinal ganglion cells.
They bundle together to form the optic nerve.They don't just report the amount of light, they report visual info too.
172
Explain the reason that photoreceptors attending to a darker part of a visual space compared to a lighter part of a visual space are depolarised, whilst the inverse is hyperpolarized
Photoreceptors respond to light exposure with graded hyperpolarisation.This results in a reduction in glutamate release at their synaptic terminals in the presence of light - cell is hyperpolarised.In a darker area where glutamate is higher, depolarisation will occur due to the excitatory effects of glutamate.
173
Outline the basic process of what happens when an image is seen.
Eyes projects and image onto photoreceptors.Photoreceptors translate into a spatial pattern of glutamate release.Bipolar cells convey signals from cones to RGCsRetinal ganglion cells send to the brain using APs
174
Who did an experiment to discover that there where two types of bipolar cells?
Keffer Hartline.
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What are the two types of bipolar cells?
ON: depolarised by a flash of lightOFF: are hyperpolarised by a flash of light
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What are the two types of synapses that bipolar cells have?
Sign inverting synapse.Sign conserving synapse.
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Outline sign inversing synapses.
They express a metabotropic glutamate receptor.Glutamate activates signalling cascade.CLOSING cation channelsWhen in light, glutamate signal is reduced, ability to close channels is descreased.Bipolar cells depolarises.
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Outline sign conserving synapse.
Express an ionotropic glutamate receptor.Cation channels OPENED by glutamate.In light, glutamate signal is reduced, channels close.Bipolar cell hyperpolarises.
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Briefly outline horizontal cells.
Cell bodies in inner nuclear layer.Synapses in outer plexiform.Allow information flow in the horizontal axis (apposed to up/down)
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Outline Tortson Wiesels study into centre surround antagonism.
Took recordings from a single retinal ganglion cell:A - small spot of light = lots of AP generation.B - BIg spot of light = Less AP generation.C - Anubus (spot of light with darkness in the middle) looks like an off ganglion cell.
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What did Torston Wiesels study do? Briefly explain why.
Provides evidence for centre surround theory due to horizontal cells:Horizontal cells link cones in a region to the retina.- Inputs from local cones sign conserving: hyperpolarised by light.- Outputs sign inverting: antagonise the light response
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Outline how horizontal cells enhance differences in diffuse light (large light spot).
Neighbouring cones are hyperpolarised.Horizontal cells become hyperpolarised.Signal (reduction in glutamate) from centre cone to bipolar cells damped.
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Outline how horizontal cells enhance differences in light spot.
Neighbouring cone are depolarised.Horizontal cells become depolarised.Signal (reduction in glutamate) from centre cone to bipolar cells enhanced.
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What do amacrine cells do in reference to information processing?
They provide an inhibitory link between bipolar cells and retinal ganglion cells - allows further modulation of response.
185
What did Horace Barlow find out about retinal ganglion cells?
The response of the retinal ganglion cells to spots of light is altered whether you're looking at it moving from bottom to top or from top to bottom.
186
Briefly outline circadian rhythms
They are 24 hour variations in physiology and behaviour.They persist in the absence of any cyclic cue from the environment.They need some external factor to keep the internal clock/rhythm in check.
187
Outline how a study into mimosa revealed circadian rhythms.
Two plants.One exposed to light, one in a box separated from external cues.Both plants had their leaves open in day time (presence of sunlight)Both plants curled their leaves at night (to conserve water)Both displayed circadian rhythms - the one without the cues proves the existence of a rhythm.
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What is the difference in ambient illumination at midday compared to mignight?
10^9 more light at midday.
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What is the most reliable environmental signal of time-of-day?
Ambient light.
190
Briefly outline the study into effects of light on rodent clocks.
Mice in a cage with a wheel - they love running on it at night as they are nocturnal.3 conditions:- normal light times (8am to 8pm)- condition 2 (00am to 12pm)- condition 3 (no light)Study measures spins on the wheel as a measure of 'night time nocturnal activity'.1. In the usual 8am-8pm, mice's activity on the wheel was greatest in the hours of dark outside of this window.2. When the light pattern was changed after a period of time, mice's wheel running activity shifted to the new 'night time' 12pm to around 8pm.1. In the presence of normal light pattern, behaviour returns to normal pattern of running outside the 8am-8pm light period.3. When there is NO light, the running activity of the mice slowly shifts earlier every day, showing that mice have an internal rhythm that is lower than 24 hours.
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What are 24 hour variations in behaviour and physiology produced by?
Endogenous circadian clocksSynchronised light:dark cycles.
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What modulates circadian rhythm in mammals? Where is it located? What does it rely on for light information?
Suprachiasmatic nucleus (in the hypothalamus)It is positioned above the optic chiasm and is innervated by the optic nerve..Receives information from the optic nerve from the retinal ganglion cells (a small % that measure ambient light).
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At the beginning of what period of night are the rod cells saturated? What does saturated mean in scientific terms?
At the beginning of twilight.It means the rod cells are fully hyperpolarised.
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What range of light intensity do cones cells cover from fully depolarised to fully hyperpolarised? What does this mean for the cones?
Over 1000xThis means that there needs to be a mechanism to allow the relative shifting of light range that cones can detect before becoming saturated.
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ADD PHOTORECEPTOR ADAPTATION DIAGRAM WITH PREMIUM
D
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Outline the changes in relationship between light intensity and photoreceptor polarisation.
Under dark adapted conditions, even relatively dim light drives full hyperpolarisation.Under light adapted conditions, photoreceptor can be partly depolarised even under much brighter light.
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What does 'adaptation' of cones allow?
Adaptation allows cones to report changes in light intensity over space and time under all lighting conditions.(Allows cones to shift sensitivity to the new level of ambient light intensities as it increases from the night to day time).
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What does bilateral enucleation mean?
The removal of both eyes.
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Outline the study into a house sparrow with the bilateral enucleation condition.(insert actogram with premium)
House sparrow with both eyes removed tested to see its circadian rhythms, measured by its perch hopping behaviour (hops in daylight).Two conditions:1 - No light2 - Day light (~8am-8pm)1.No light, perch hopping behaviour starts later every day (the birds get up later everyday) for the whole condition. Shows circadian rhythm is longer than 24 hours.2. Consistent light. The perch hopping behaviour starts every day at the start of the light and ends at the end of the light. They have no eyes, yet they manage to set their circadian rhythms to the light provided.This suggest extraocular circadian rhythm detection.
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Outline the study into a house sparrow with the bilateral enucleation condition + black ink under scalp.(look at lecture slides for actogram)
1. Consistent light. The perch hopping behaviour starts every day at the start of the light and ends at the end of the light. They have no eyes, yet they manage to set their circadian rhythms to the light provided.2. Black ink injected under scalp.Circadian rhythm no longer set to light, birds get up later everyday and goes to their innate > 24 hour circadian rhythm.This shows that there is some extra-retinal photoreception occurring underneath the scalp: the photoreceptors synchronising the clock must be in the brain.
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What is the result of bilateral enucleation in mammals? What does this show>
Abolishes all responses to light in mammals.This shows that 'time of day' responses originate in the retina.
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Outline the study in mice to figure out which cells (other than rods/cones) are photoreceptors.
Rodents with rods and cones knocked out to test whether they will express circadian rhythms without these photoreceptors.They measured the pupil responses in these mice in response to light.(ADD PIC WITH PREMIUM)It was found that in dim light the pupils were large, and in light they were small.Therefore, even without the rods and cones, there is still photoreception to detect the light in the environment and bring about physiological changes as a result.
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Outline the study in which dye was injected into the SCN, what was it trying to find?
SCN is where the circadian rhythm is modulated.By injecting dye, the connections from the eyes will be revealed retrograde (back along the path) to where the ambient light information originates from.This dye travels down axons of retinal ganglion cells and labels >1% of all ganglion cells.
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What occurred in the two types of retinal ganglion cells when removed from the retina and exposed to light?
ON retinal ganglion cells still show light response when removed from the retina.All other retinal ganglion cells didn't respond by themselves.
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Outline the retinal ganglion cells that project to the hypothalamus.
They are photoreceptors and they depolarise to light - detect ambient light levels.
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What do the amino acid sequences of opsin like proteins in vertebrate genomes indicate about them?
Shared evolutionary history with rod and cone opsins.They are membrane associated.They are GPCRs They bind chromophores.
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What is a common opsin between non-mammals and mammals non-rod/cone photoreceptors?
Melanopsin.
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What was the beginning proof that melanopsin is relevant in ambient light detection?
Melanopsin is in the retinal ganglion cells that project to the hypothalamus.
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Outline briefly the two gene studies into melanopsin.
In mice, those with a melanopsin knockout had no RGC's that respond to light.Suggesting that melanopsin is key in ambient light detection.Add melanopsin to see if it brings about light sensitivity in a nerve cell that is not light sensitive (Neuro2A - mouse neuroblastoma)This makes cells light sensitive.Shows that melanopsin does make cells light sensitive.
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What is the Thalamus (basic structure)
- Large structure - divided into multiple nuclei with distinct functions (some visual, some non-visual)
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What is the Lateral Geniculate (basic structure)
- Primary visual part of the Thalamus- Vast majority of RGCs (around 90%) project here in primate
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Where can the Thalamus be found and what does it connect?
It is part of the Diencephalon - connects the midbrain to the cerebral hemispheres
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What is the basic role of the Thalamus (3)
- Receive information from the periphery- Process and communicates to cortex- Essential link in transfer of sensory information
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How many cone types does the human retina have? What is the difference between them
3They are maximally responsive to different parts of the spectrum.
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Outline the mechanism behind the basis of colour vision.
Comparing between the cones spectral sensitivity allows us to perceive the spectrum of colour:Red vs GreenBlue vs Yellow (which is red and green cones)
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What is colour perception about?
Observing the ratio between your colour photoreceptor activity.
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What wavelengths does the visible spectrum run between?
roughly 400-700nm
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What are the two mechanisms for achieving colour vision?
Colour opponent centre : surround (green vs red)Colour opponent ON and OFF bipolars (blue vs yellow)
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Briefly outline Opsin proteins
7 transmembrane domain G protein coupled receptorBinds retinaldehyde and determines the spectral sensitivity of it.Translates isomerisation of retinal into a 'biological' signal.
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Retinal ALWAYS absorbs light, if retinal is always the same in each opsin, then how are different cone cells sensitive to different wave lengths of light?
Retinaldehyde is most sensitive to UV light.When retinaldehyde is bound to an opsin, the amino acids that surround it change the set electrochemical state of the retinal, which changes the efficiency of light absorption of the retinal.
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What is a function of opsin that is related to retinaldehyde?
One of the functions of opsins is to change the wavelength sensitivity of that retinaldehyde and determine the spectral sensitivity of that light absorbing event.
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What wavelengths do the rod opsins change retinaldehydes spectral sensitivity to?
From UV to around 500nm
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What wavelengths do the each of the cone opsins change retinaldehydes spectral sensitivity to?
Long-wave (red) - 564nmMiddle-wave (green) - 533nmShort-wave (blue) - 433nm
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What determines our perception of colour and what determines that factor?
The cone opsin amino acid sequences.Which are encoded by out genome.
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Which two opsins are X-linked in humans?
LWSMWS
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What causes red:green colour blindness (think process - not gene)
Lack colour opponency of R/G due to lack of opsins.
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How many cones opsins do chickens have? Name all their opponent processes.
4Red/greenBlue/yellowGreen/cyanCyan/violet
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What two things would adding cone types in a human allow?
Improved spectral resolution within human visible range.Potential extension of vision into UV range.
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How many cone opsins do most animals have?
2 cone opsin genes middle wave (green) - 510 nmshort wave (blue) - 360nm
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What causes inter-individual and inter-species differences in colour vision?
The number of cone classesTheir spectral sensitivity
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What does the thalamus determine
Determines whether or not information should reach conscious awareness and is involved with sleep/wake and attention
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Relationship between thalamus and cerebral cortex (how do they work together)
- Sends information to CC for all sensory systems other than olfaction- Every relay nucleus received information back from cortex- Feedback may be specific or diffuse, may separately target relay cells and interneurones.
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How many layers make up the LGN
6 Layers or Laminae
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What are the names of the layers of the LGN
1 and 2 = Magnocellular (large cells)3 to 6 = Parvocellular (small cells)
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Organisation of LGN layers: I (structure of layers)
* Each cell received most of its retinal input from a single retinal ganglion cell* Each layer contains both excitatory (relay) cells and local inhibitory interneurons* Very small excitatory relay cells underneath each laminae
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Organisation of LGN layers: how do retinal projections work
• Retinal projections are retinotopically ordered - each LGN gets signals from RGCs viewing the opposite visual hemifield, and within each layer adjacent cells view adjacency portions of visual space.
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What is a receptive field of a sensory neuron
A region of space in which the presence of a stimulus will alter the firing of that neuron (identified for auditory system, somatosensory system and visual system)
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For an On-centre retinal ganglion cell what will happen if the centre is fully covered by light and the surrounding is partially covered
Cell is still excited
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For an On-centre retinal ganglion cell what will happen if the centre is fully covered by light and the surrounding is also fully covered
Nothing - firing rate will remain the same
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What does a small receptive field cause?
High spatial acuity - so more detail
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What does a large receptive field cause?
Low spatial acuity - less detail
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Parvocellular LGN neurons - (8 things specific to Parvo)
- Dorsal 4 layers have smaller cell bodies- Small receptive fields- High spatial acuity- Prefer low temporal frequencies (slow changes)- Receptive fields have concentric centre/surround like the retina- Both On and Off centre subtypes-Chromatic (red/green) but can respond to brightness- Input from retinal P ganglion cell
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Magnocellular LGN neurons - (8 things specific to Magno)
- Ventral 2 layers, have larger cell bodies- Larger receptive fields- Lower spacial acuity- Prefer high temporal frequencies (fast changes)- Receptive fields have concentric centre/surround like the retina- Both On and Off centre subtypes- Achromatic- Input from retinal M ganglion cells
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Outline 6 things specific to Koniocellular LGN neurons.
- Newest addition to the family- Very small cells found between main laminae- Direct input from blue/yellow RGCs- Indirect input from superior colliculus- Heterogenous types- functional properties/function largely unknown
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Relay cells (mechanism and where they can be found)
- 90% of LGN cells are relay, single axon projects to V1- Use glutamate: are therefore excitatory - Each has an axon collateral just above the LGN - terminates in the visual sector of the TRN, known as the: perigeniculate nucleus (PGN)
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Which neurotransmitter do all inhibitory cells use
GABA
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Noradrenaline (Wheres is it produced and whats its role)
-Produced in locus coeruleus (LC)- Maintains vigilance, fight or flight responses - Extensive projections including thalamus + cortex
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Acetylcholine (whats its role)
- Basal forebrain groups: innervates entire cerebral cortex including amygdala and hippocampus- Pontine groups: innervate brainstem reticular formation and thalamus- Important for arousal and REM sleep
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Serotonin (where is it found and whats its role)
- Serotonin cells found in the Raphe nuclei- Pone and midbrain groups project the whole of the forebrain - Role in mood, cardiovascular control, thermoregulation, modulate thalamic and cortical function
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Dopamine (whats its role)
-Multiple cell groups, some of which provide input to thalamus- Roles in reward, neuroendocrine, motor control- Thalamic projections mainly avoid primary sensory areas
251
Briefly outline visual processing in the brain.
Occipital lobe is the primary location for visual processing.Most parts of the brain process visual information in some way.
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What is the basic cortical structure?
6 layer structure, with some sub-lamination in layer 4 in visual cortex
253
Outline the role of Nissl staining in identifying cortical structure.
It tells you about the size and density of neurons by staining (highlighting) the cell bodies.
254
Outline the role of golgi staining in identifying cortical structure.
It's important because it helps us understand the connections between neurons and how signals move between/across layers.
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Why is the fact that there is a low probability of cells up-taking golgi stain a benefit?
It allows a more detailed morphology of those cells (doesn't get too crowded).
256
How can cells in the cortex be classified?
Based on morphology (shape) of the cell body, or distribution of dendrites or axon terminations.
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What does 'cell types are ubiquitous' mean in reference to the cortex?
The types of cells found in one area (i.e. visual cortex) applies to most of the cortex - not distinct to any given cortical region.
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What are the two main types of cortical cells and why are they called their names?
Pyramidal cells: cell body resembles a pyramid shape.Stellate cells: have star shaped cell body and projections.
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Outline what would be found when looking at the detailed morphology of cortical cells - why would this be a benefit?
'Spiny' dendrites would be seen at higher magnifications.- Increases the surface area for synaptic contact.- allows for local computation.
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What is meant by local computation in reference to cortical cells?
It allows for the calculating of inhibitory vs excitatory inputs locally so that information can be modulated/decided whether or not this information should be transmitted to the cell bodies to bring about a change.(e.g., if there is a balance between +/- then information doesn't need to be passed on)
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Outline 3 ways of understanding the location and properties of cortical cell types.
- Record electrophysiologically to define sensory properties.- Fill with dye to determine morphology.- Counterstain (e.g. Nissl) to find laminar position
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Outline spiny neurons.
>80% of cortical cellsglutamatergicall excitatory(mainly pyramidal but some are stellate)
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Outline non-spiny cells
<20% of cortical cellsGABAergicinhibitory interneurons(a vast array of different cell types)
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Outline a summary of excitatory cortical cells.
Shape:- Pyramidal (layers 2/3, 5, 6)- Stellate (4)Spines:- SpinyTransmitter:- GlutamateTargets:- Both local and distant
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Outline a summary of inhibitory cortical cells.
Shape:- Stellate, fusiform, bi-tufted etc.Spines:- Aspiny (smooth)Transmitter:- GABA (and peptides)Targets:- Local
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What are the three subdivisions of the layers in the cortex?
1, 2, 3 = Supragranular4 = granule cell layer5, 6 = Infragranular
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Outline the properties of the layers of the supragranular layer.
Layer 1:- cell sparse, dendrites and axons.Layer 2:- mainly small pyramidal cells (the extra granule layer)Layer 3:- variety of cell types, many pyramidal, deeper in the layer (the external pyramidal layer)
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Outline the properties of the granule cell layer.
Layer 4:- Primary spherical cells (sub layers A, B, C)
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Outline the properties of the layers in the infragranular layer.
Layer 5:- cells typically larger than layer III(internal pyramidal cell layer)Layer 6:- heterogeneous mix(polymorphic or multitform layer)
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Outline where the inputs from the LGN go within the visual cortex.
Primarily to layer 4:- Parvo to cortical layer 4Cbeta - Magno to cortical layer 4CalphaA copy of the input signal also goes to layer 6.
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Outline where the signals from layer 4 go within the visual cortex.
Go to layer 2/3:- Parvo from 4Cbetato layer 2/3- Magno from 4Calpha to 4B, then to layer 2/3
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Outline where signals from the koniocellular input go to.
Straight to layer 2/3
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Would outline local cortical circuits and cortical outputs for visual cortex but looking at slides will be more efficacious - so go and look at powerpoint to understand/revise this.
Cheers people
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Outline the areas in which cortical magnification occurs.
The retina, LGN and the visual cortex - fovea being most represented
275
Outline the organisation of visual inputs from the LGN to visual cortex (think ocular dominance).
Eye-specific LGN layers project to separate 'zones' in the cortex- These are sorted into 'ocular dominance columns' in which there will be separate columns for each of the eyes.- These inputs are separated at layer 4 and binocular divergence doesn't begin until layer 2/3
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What is 3^H-Proline and what is its relevance?
It is a radio labelled amin-acid that was injected into one eye of primates and transported via the LGN to the V1.- It revealed a 'zebra-stripe' pattern of layer 4 showing that the zones receive input from the injected eye every ~500um.
277
Outline the importance of Hubel & Wiesel.
They researched visual fields and centre:surround antagonism by primarily studying cat's visual cortex's
278
Outline V1 'simple cells'.
Mainly in layer 6- have separate ON and OFF subregions- elongated receptive fields- wide variety of orientations & arrangements
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How do simple cells get their receptive fields?
Convergent inputCentre:surround inputs from the LGN determine the receptive fields - 1 simple cell represents the visual fields of multiple LGN cells. (look at powerpoint if this doesn't make sense).
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How are simple cell receptive fields useful? Briefly outline how they work.
They respond to light:dark edges with specific orientations - makes them good at detecting edges of a particular polarity.If the light covers the ON centres then it will excite as it is right orientation to cover these parts.If the bar is the wrong orientation it will inhibit as it covers OFF centres.
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Outline V1 'complex cells'
Layer 2/3They respond to 'any' edges with correct orientation.They have convergent input from multiple simple cells with similar orientation but different subunit arrangement (there will be ovelapping layers of OFF/ON).This means complex cells visual fields are 'speckled' with OFF/ON regions.
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Outline 'hypercomplex' cells.
Only respond to bars/edges of specific lengths.They are NOT a unique cell type:- A subset of both simple and complex cells that express 'length tuning'- Useful for detecting corners/curved edges.
283
Outline the V1 organisation of orientation tuning.
There is a oscillation of preferred orientation ACROSS layers (preference slowly rotates as you go across)/Preferred orientation is maintained vertically BETWEEN layers.Finding the peak orientation of a cells tells you about the preferred orientation of neighbouring cells.
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What did Hubel & Wiesel suggest in their 'ice-cube' model of V1 organisation?
For any point in space there should be a set of orientation columns for each eye.
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What is 'like-like' connectivity in reference to intercolumn connectivity?
Lateral communication between cells with the same preference:- Warns neighbouring cells about moving stimuli.
286
What is cytochrome oxidase (CO)?
It is a marker of cellular activity.
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What did CO reveal about V1 organisation?
Blobs in layer 2/3 that are regularly spaced across the cortical surface.
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Outline information about the cells in the 'blob' regions of layers 2/3 in V1.
They are poorly tuned for orientation but are colour tuned.- Koniocellular and Parvocellular neurons are both colour sensitive so the combine in the blob regions to make cells that are tuned to colour.
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Outline cortical modules in V1.
For every point in space there is a cortical module in V1 which has 'hypercolumns':L and R hypercolumns:- a central region that processes colour and a set of orientation columns that 'pinwheel' out from the centre.
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What is amblyopia? (2 definitions)
Impaired or dim vision without obvious defect or change in the eye.(brain is the source of the problem).The absence of adequate symmetrical stimuli to the two eyes so that binocular reflexes cannot be developed - (something that happens in development that stops the eyes from working together).
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What is the basic cause of amblyopia?
Anything that leads to imbalance or mis-integration of the input to TWO eyes.
292
Outline the study into the effects of monocular deprivation on ocular dominance columns in V1 (monkey study).
Suturing one eye shut soon after birth, blocking vision to that eye.Let the monkey grow up and then test the effect it had on V1 years later.Results in wider of ocular dominance columns for the non-deprived eye.
293
Outline the timings of monocular dominance and how they are critical.
3^H-Proline injected into non-deprived eye and transported via LGN to the V1Eyes closed at 'x' for 14-18 months:2 weeks old: large ocular dominance for non-deprived eye.5 1/2 weeks old: large ocular dominance for non-deprived eye.10 weeks old : still dominant for non-deprived but less exaggerated.14 months old: seemingly has no effect - ocular dominance columns are equal.
294
Outline the Hubel and Wiesel ocular dominance scale.
Graphs to quantify the electrophysiological responses of V1 cells to stimuli applied to the left or right eye.NORMAL: Shows 'bimodal' distribution of activation. Number of cells activated highest at the extreme contra/ipsilateral regions.MONOCULAR DEPRIVATION:Shows heavy monocular dominance to the side without deprivation - highest activation of cells at this extreme, relatively low/flat in all other places.(look at notes for graphs if confused).
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Define contralateral and ipsilateral.
Ipsi = same sideContra = opposite side
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Outline the critical periods in relation to monocular deprivation in the cat, macaque and man.
Cat:- three to four months.Macaque:- 1st six weeks high susceptibility.- 10 weeks requires longer period of deprivation.- No effect is carried out after one year.Man:- up to 5-10 years.- most pronounced during first years.
297
Outline the study into functional changes in V1 following monocular deprivation.
Experiment took signals purely from non-functional eye.Initially showed no activity.Introduction of Bicuculline (GABA antagonist) which stops the inhibitory actions of GABA then showed activity of these cells.Shows that signals from the deprived eye are actively supressed by local interneurons.
298
What are the two types of stroke?
Occlusive and Haemorrhagic.
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Outline occlusive strokes.
>80% of all strokes.- Due to closure of a blood vessel.- Blood clot.- Atherosclerosis.
300
Outline haemorrhagic strokes.
RARE- due to a RUPTURE of a blood vessel.- hypertension, aneurysm.
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What is a scotoma?
A blind or partially blind spot in the visual field (e.g., caused due to stroke affecting V1).
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Give a general description of the types of scotoma (4 types).
absolute - no remaining visionrelative - some remaining visionhemianopic - one half of the visual field gonefacultative, suppression- in alternating foveation in squint conditions
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What is the name of the artery that feeds V1 on both sides? What can occlusion of it cause?
Posterior cerebral artery.Lack of blood flow to a whole V1 on one side of the brain and therefore a widespread loss of vision.
304
What is homonymous hemianopia? What is interesting about it?
Loss of vision on the same side in both eyes (visual field).Even though you can't 'see' half of the world, your eyes will still track the area that you cannot see.
305
What is meant by blindsight?
When people aren't completely unresponsive to the part of vision that they cannot see.
306
Outline blindsight (reasons, how it is expressed etc).
Results of extensive damage to the striate cortex.Patients asked to locate in visual field that they can't see will claim to be blind, yet when asked to guess, they will get it right higher than the frequency chance suggests.
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What were the first suggested mechanisms of blind sight?
Portions of the V1 remain intact and active.Residual vision in higher cortices (routed through the superior colliculus/pulvinar).
308
Outline the basic V1 lesion study into blindsight.
Grid with red spot in centre bottom, then 4 squares, one in each corner.Half the screen will be in blind hemifield, half in good.Test to see whether monkeys can still identify the target location even in blind side.The lesioned monkeys still were good at detecting what they shouldn't be able see. - High % right shows some kind of vision capabilities.
309
Outline the complex V1 lesion study into blindsight.
NORMAL trials: target appears in one of 5 locations in the 'good field – touch targetBLANK trials: no target appears - touch the outlined rectangle on the upper leftPROBE trials: a target appears in the blind field - touch this target. RESULTS:- During probe trails – lesioned monkeys respond as if no target had appeared.This shows that although visual information gets through, they won't assume they can see it unless prompted.
310
Briefly outline Zihl's patient.
They had motion agnosia - intact visual field but lost all perception of movement (e.g., people would 'spawn' into the room).Due to bilateral damage to the human homologue of V5 (MT).
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What is neglect?
Damage to the parietal cortex - the 'Where' stream.
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What happens in people with the most extreme forms of neglect?
They 'lose' perception of one half of the world.E.g., trying to fill a glass that they can see and pouring the water out 30cm to the left.
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What's the difference between hemianopes and neglect patients?
Hemianopes:- they scan the entire scene but can't see the side (e.g., left(Neglect patients:- only view the hemispace contralateral to their lesion (ignore the opposite side of the world)
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What would a neglect patient do with the following situations?- Straight line bisect- Bisects of short lines across a visual field- Draw the hours on a clock
1. Bisect it heavily to the side opposite the lesion.2. Will only bisect the lines in the field they can see.3. Will write all the numbers on one side of the clock.
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What is meant by neglect is seen in a supra-retinal reference frame?
Neglect doesn't only stop you from seeing things in-front of you, it limits your ability to perceive that part of the world existing (think duomo, they didn't even register the side of the world that they have neglect, until they changed the position of their perception).
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What damage causes neglect?
Parietal, most commonly right parietal damage.
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What, other than damage, could neglect be caused by?
Competition (actively shutting off one half of the V1)Inability to disengage attention.
318
What is prosopagnosia?
An object agnosia, you don't recognise objects but can identify via other modalities.E.g., don't recognise face, but can identify via voice.
319
What occurs due to stoke damage to the inferior temporal cortex? Which stream is this?
What stream.Can identify a face as a face, or parts of faces, or even emotions on facesCannot recognise individual people, even close family members (potentially even their own face)Identities are not lost, only the connections between particular faces and identities
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What are the 2 main visual pathways in the brain called and what are they responsible for
Dorsal stream “Where” - where things are in the world, gives information on the location of objectsVentral stream “What” - identifying objects and distinguishing between people or objects.
321
Is the MT myelinated or not and why?
MT (V5) has strong myelination which is important because processing motion needs to be fast so that the brain can respond quickly
322
What are the Motion pathways properties (Where does it receive input from and describe the receptive fields):
Mainly magnocellular input :- low spatial acuity, high preferred temporal frequency- Via special projection from layer 4BAlso receives indirect from layer 2/3 in V1:- Via “thick stripes” in V2Receptive fields are:- Much larger than V1- can also detect colour- direction selective
323
Provide a summary of direction tuning
Motion in plaids is made up of components:- different directions of motion- different orientations - but it is perceived as composite Most cells in V1 and V5 are component selective20% of V5 cells are selective for composite stimulus - generate perceived motion
324
What is a plaid
A stimulus of 2 superimposed sine-wave gratings moving in independent directions
325
Medial superior temporal cortex (MST) - What are the receptive fields like and what does it respond to?
MST cells have much larger receptive fields that V5 - sums input from V5Respond to direction of stimulus motion but can be complex - expansion, contraction, circular or spiral.
326
What does the LIP stand for
Lateral Intraparietal cortex
327
What are the receptive fields properties in LIP
- Cells do not care about colour or form (orientation)- Retinotopic receptive field has a “motor field”- Cells are much more responsive to a stimulus in the receptive field if these are the target of the saccade.
328
Describe the sensory coding in LIP
- For every region of visual space, there are many cells which represent that location - Among cells representing any one location each may have a different “gain field” with respect to head/eye position- The population of LIP cells therefore codes the positions of objects in space with respect to the body
329
What does the LIP have to make sure it has 1 representation of the world and not 2
Strong callosal connections with LIP in the other hemisphere
330
Why do LIP cells have very large axonal and dendritic arbours
Need to pool information across large areas
331
What information allows the LIP to coordinate movements to locate objects
It combines information from the retina, eye position, head position, body position.
332
Whats the benefit of LIP cells having memory
Allows us to decide what to look at next (for example if you are speaking to someone and you see something in your peripheral, you can wait and look after because of memory)
333
Whats the order of the 4 areas in the "what" pathway (temporal)
V1-V2-V4-Inferior temporal lobule
334
What is sound?
A displacement of air that creates regions of compressed air (peaks) and rarefied air (troughs).
335
What does a high frequency translate to? (sound)
Higher pitch (shorter wavelength)
336
What does high intensity translate to? (sound)
Louder volume (increased distance between peaks and troughs)
337
What is the speed/velocity of sound at room temperature?
343m/s
338
What is the equation for velocity and what is it measured in? (sound)
frequency x wavelength = velocity (m/s)
339
What does wavelength mean? (sound)
Distance between successive peaks (in metres)
340
What does frequency mean? (sound)
Numbers of peaks per second (in Hertz)
341
What are the three parts of the ear? What are their component parts?
Outer ear:- Pinna (the outer ear structure we know as the ear)- The auditory canalstops at tympanic membraneMiddle ear: the ossicles- Malleus - Incus- Stapesstops at the oval windowInner ear:- vestibular system- cochlea
342
What medium does sound travel better through - air or fluid?
Air
343
Which region of the each is filled with fluid?
The cochlea.
344
What are the bones in the ear called? What is their role?
The ossicles (Malleus, Incus, Stapes), they amplify the sound intensity at the oval window to compensate for the air-to-fluid dilution of sound.
345
Outline the function of the middle ear (include the steps).
When air displaces the tympanic membrane, it pushes the handle of the malleus.The malleus acts as a level with a fulcrum point that is nearer to the 'handle'As the handle is displaced to the right, the head is displaced to the left.The malleus passes this movement to the incus and the incus to the stapes.Due to the lever effect, pressure at the oval window is increased x20.
346
What are the three mediums sound travel through to be processed?
Air -> Mechanical -> Fluid.
347
What are the tensor tympani and stapedius muscles? What is their role?
Tensor tympani is attached to the malleus and the stapedius is attached to the stapes.When these muscles contract, they stiffen the ossicles and dampen the sound intensity that enters the inner ear via the oval window.This occurs with high volume low freq sounds to prevent damage to the hair cells in the inner ear.
348
What is the attenuation reflex?
It is when loud low frequency noise activates descending (effector) reflex circuits to dampen sound input to protect the hair cells from mechanical damage.High intensity (>60dB)Low frequency (<2000Hz)DOESN'T WORK ON SUDDEN LOUD NOISE
349
Outline the two potential pathways of the attenuation reflex.
1:- Hair cells send signals through the auditory nerve to the PVCN, which then sends it to the SOC.- This passes the information on to the facial motor nucleus which then sends the signals down cranial nerve 7 (facial nerve).- This feeds back to the stapes to contract and dampen the stapes movement and reduce the displacement of the oval window.2:- When talking or chewing, to dampen the sound the motor V nucleus signals to cranial nerve 5 (trigeminal nerve to the tympanic membrane.- The tympanic membrane as a result will contract to pull on the malleus to tighten the membrane and dampen the noise.
350
Outline the structure of the inner ear
Three fluid filled chambers:-Scala vestibuli and scala tympani: filled with perilymph and either side of the scala media- Scala media: in the middle and filled with endolymph.The organ of corti:- this is where the inner and outer hair cells are (below the tectorial membrane)- sits on the basilar membrane between the scala media and scala tympani
351
What is the ionic make up of perilymph?
140mM Na+7mM K+
352
What is the ionic make up of endolymph? Why is it this way? Why is this significant?
1mM of Na+ 150 mM K+The stria vascularis takes sodium out and pumps potassium in.It's important because K+ is what causes the cells to release neurotransmitter.
353
Outline the structure of the cochlea
The basilar membrane runs down the middle between the chambers: scala vestibuli and the scala tympani.The basilar membrane at the top (base) it is thick and narrow, at the apex it is thin and wide (gradient between these two points).Sound enters in the oval window, down the scala vestibuli, through the helicotrema (apex) and back round through the scala tympani to the round window.
354
Briefly outline how the cochlea works (process).
Stapes taps on the oval window, causing sound waves in liquid to pass through the perilymph, which deflect the basilar membrane.The sound waves travel down to the helicotrema and to the round window where they are dampened.Highest frequency will deflect near the base, lower waves near the apex.
355
Briefly outline the tonotopic organisation of the basilar membrane.
There is a gradient of frequencies that causes maximal displacement of the basilar membrane.High frequency -> Low frequency Top -> bottom (apex)
356
Outline the positioning of inner and outer hair cells in the organ of corti.
Outer hair cells have their stereocilia buried in the reticular lamina- Their stereocilia are arranged in a V shape.Inner hair cells have free stereocilia that sit below the tectorial membrane.
357
Outline the mechanical displacement of hair cells.
Outer hair cells have their stereocilia embedded in the tectorial membrane and the inner hair cells have a gap.When the membrane vibrates and moves up, it pushes up on all the cells and the stereocilia contact the membrane, causing them to bend.Mechanical displacement of the hair cells is what causes them to detect certain sound waves.
358
What is the relationship between the deflection of hair cells and their receptor potential?
Deflection of the stereocilia in one direction increases receptor potential Deflection of the stereocilia in the opposite direction decreases receptor potential
359
Outline in depth the tips of hair cells.
The tips of the stereocilia of hair cells have mechanically-gated TRPA1 ion channels.TRPA1 channel has a tip link which is a spring mechanism that links it to the adjacent stereocilium.There is a small amount of K leakage into the cell when unstimulated.When the hair cells bend towards the kinocilium, the tip links open the cells and the high K+ conc endolymph makes it a high % chance of depolarised.When the cells are bent the other way, blocking any entry of K+, this causes a slight hyperpolarisation as no leakage can come in.IF bent in the right way, the high K+ influx depolarises the cell, causing voltage gated Ca2+ channels to open, leading to neurotransmitters to be released (think SNARE proteins) = activation of spiral ganglion cells.
360
Where is the first place of depolarisation in the process of audition?
Spiral ganglion cells.
361
Outline the difference of innervation of SGC's and outer/inner hair cells.
Outer hair cells have a poor innervation of SGC'sInner hair cells have a dense innervation of SGC's and can activate multiple of them.(inner hair cells are the ones that do the sound detecting)
362
What is the importance of SPC's and why are there so many at the base of inner hair cells?
- They have different ability to fire (based on intensity)- Different sensitivities to receiving neurotransmitter from the hair cell- Some fire without the presence of sound (these are the ones that respond to low sound).
363
Outline the coding of sound intensity.
Different types of SGC's fire at different volumes/intensities.High spontaneous rate (low threshold:) SGNs fire from 0dB up to ~20dB saturationMedium spontaneous rate (mid threshold): SGNs fire from ~20dB up to ~40dB saturation Low spontaneous rate (high threshold): SGNS fire from ~40dB to ~80dBCells don't fire more than their maximal rate, therefore having different sensitivities for SGC's allows for the coding for different volumes.When a low decibel sensitive SGC is firing maximally, it is the presence of ones with a sensitivity above this range that allows detection of all volumes.
364
Outline the interaction between hair cell and SGC's to code for the frequency and volume of a sound.
The frequency of the sound is coded by the hair cell that is being activated due to the basilar membrane at that particular freq.As the sound wave comes in through cochlea, it will cause the basilar membrane to maximally vibrate at the region where this freq specific hair cell sits.That hair cell will send it to the spiral ganglion neurons.If it’s quiet, it will only stimulate the low frequency ones, when the volume is higher, it will vibrate the basilar membrane more and therefore stimulate firing in the high threshold ganglion neurons.Frequency coded by hair cell.Volume coded by spiral ganglion cell that is firing.
365
Outline the cochlea amplifier.
Outer hair cells are attached to the basilar membrane and reticular lamina They have a motor protein (prestin) that allows them to elongate or compressWhen these cells are activated by K+ influx it activates motor proteins that compress the cell. This amplifies the basilar membrane movement (x100) and leads to increased bending of inner hair cell stereocilia This is what amplifies the sound as less stimulation of the basilar membrane is now needed to displace the hair cells and let K+ influx.
366
Outline the process of Medial Olivocochlear Reflex inhibition.
Protective mechanism for a loud high frequency noise:The problem with loud and high frequency sound, it can over bend the stereocilia which can cause them to break and therefore causing permanent hearing damage.When you get high volume and frequency sound, it switches off the amplifier to allow more movement before damaging the inner hair cells.Inner hair cells send a signal to the PVCN which then signals to the VNTB on the contralateral side.This sends an axon via the medial olivocochlear system which releases acetylcholine onto the outer hair cells which hyperpolarises them so when K+ comes in and wants them to compress, they instead stay upright.This means that the the distance between the membranes stays large so that the loud noise won’t break the inner hair cells.
367
What is conductive hearing loss and how do you test for it?
It is a defect in the outer or middle ear.Checked using Rinne's test
368
What is sensorineural hearing loss and how do you test for it?
Defect in the inner ear - cochlea or auditory nerve.Checked using Weber's test.
369
Outline Rinnes test.
Place base of struck tuning fork on the mastoid bone.Have a patient indicate when the sound is no longer heard.Move fork beside ear and ask if they can hear it now.NORMAL HEARING:- AC (air conduction) > BC (bone conduction) - can hear the fork by the ear.CONDUCTIVE LOSS:- BC > AC - can't hear fork by ear.
370
Outline Weber's test.
Place the base of a struck tuning for on the bridge of forehead, nose or teeth.NORMAL:- no lateralisation of hearingUnilateral Sensorineural loss:- can hear better on unaffected side.
371
Give some examples of animals can hear ultrasound or infrasound.
Can hear ultrasound:- Bats- Dolphins- Insects- Shrews (can only hear ultrasound).Can hear infrasound:- Crocodiles- Blue wales- Elephants
372
Outline what occurs when the wavelength of a sound wave is smaller than the barrier width.What two concepts are related to these phenomena?
A sound shadow is generated behind the barrier .Sound is reflected.ILD (Interaural Level Difference).Echolocation.
373
Why do bats use such ultrasound for echolocation?
Sound is only reflected if the wavelength is smaller than the barrier it hits.As bats catch small prey like flies, the wavelength must be smaller than the fly for it to be reflected off and allowing them to perceive it.
374
Why do Wales and Elephants use infrasound to communicate?
The size of a wavelength is related to the distance it can travel without dampening.Shorter wavelengths will dampen over shorter distances than longer wavelengths.Therefore they use LONG wavelengths to communicate because they want to communicate across large distances (oceans/plains).
375
What conditions in a human make it easiest to learn to echolocate?
The earlier you learn to echolocate e.g., being blind from young, makes it easier due to being more neuroplastic.
376
Briefly outline the mechanisms that allow people to learn to echolocate.
People who are blind from young have little to no use for their visual cortex as a visual processing hub (as they cannot provide information to it via the optic nerve).however, the role of the visual cortex is not only to perceive visual information, but to also create a 3D structure of the world.Therefore, the people who echolocate repurpose their visual cortex to make a 3D map of the world using the auditory information from echolocation.The repurposing is due to plasticity.
377
Outline which part of the brain deaf people repurpose and why.
Deaf people repurpose the auditory cortex - mainly the belt region - for interpreting sign language.This is because the belt region is responsible for parts of language comprehension processing.Due to plasticity, the brain can use this region to interpret sign language in the same way it would process phonemes of spoken language.
378
When does the processing of sound become conscious to us?
When it reaches the auditory cortex.
379
Where is the primary auditory cortex located?
Located on the superior temporal gyrus in the temporal lobe.
380
What are the three subdivisions of regions in the auditory cortex?
Primary auditory cortex which is the **core**.Secondary auditory cortex which is the **belt**.Tertiary auditory cortex which is the **parabelt**.
381
Outline the primary/core region of the auditory cortex.
It perceives the frequency of sounds and is mapped out tonotopically similar to the cochlea nuclei.In the ROSTRAL region you have the lower frequency soundsIn the CAUDAL region you have higher frequency sounds.
382
Outline the secondary/belt region of the auditory cortex.
The core region connects to the belt, and when information arrives here, it has a similar tonotopic organisation.Processing is more complex here as neurons begin to respond to combinations of sounds.e.g., the separate components of sound would be picked up from different regions of the core depending on their frequency, when that info reaches the belt it will start be processed in its temporal organisation to process the semantics of the sounds.Here neurons start to fire due to combinations of sounds from the core - starting the processing of the sound as language.
383
Outline what is meant by EE in the auditory cortex.
Excitatory excitatory neurons.These are found in the core at right angles to it, layered with the EI neurons, and are in regions that detect information coming in from both ears.They send excitatory signals when signals come in from BOTH ears.
384
Outline what is meant by EI in the auditory cortex.
Excitatory Inhibitory neurons.These are found in the core at right angles to it, layered with the EE neurons, and are in regions that detect information coming in from single ears.They fire excitatory signals in response to input coming in their ipsilateral ear, but inhibited by signals from the contralateral ear.(This is the same on both sides of the brain).
385
What gives evidence to the primary auditory cortex beginning to process direction of sound?
EE and EI.Firing in response to both/single ears receiving sound input.
386
Outline the rostral region of the primary auditory cortex.
It's located rostrally to the primary core (obviously).It's tonotopic organisation is the reverse of the primary core:- Low frequency on the rostral side.- High frequency on the caudal side.
387
Outline the rostral temporal region of the primary auditory cortex.
It is thought to be a mirror of the rostral region of the core.
388
How many subdivisions are there within the belt region of the core?
Thought to be around 8.
389
From what region of the auditory cortex does information begin to travel down the auditory 'What' and 'Where' streams to the frontal cortex?
From the belt region.Information also goes straight from the belt region to the destination of both these pathways:- DLPFC- VLPFC
390
Outline the Postero-Dorsal pathway.
It is the 'where' pathway.Goes through the Parietal Lobe, to the Premotor Cortex and then to the Dorsolateral Prefrontal Cortex.The information comes mainly from the caudal region of the belt and provides information about 'where' the sound came from.Information can come straight from the belt and V1 (visual information) to the DLPFC too.
391
Outline the Antero-Ventral pathway.
It is the 'what' pathway.Goes through the Temporal Lobe to the Ventrolateral Prefrontal Cortex.Information is provided about 'what' is being heard - the characteristics and semantics related to perceived sound.Information can come straight from the belt and V1 (visual information) to the VLPFC too.
392
Outline frequency and decibel maps in relation to human phonemes and the brain regions associated.
Look in your notes for the graph w the frequencies.There is an observable difference between certain letters/sounds and their frequency and volume - this changes person to person but there is a semi-set organisation.The core will identify these frequencies and the belt will combine them into perceivable words.
393
Outline Wernicke's area.
This is the region in the temporal lobe that is responsible for language comprehension.This is where combinations of words are put together so you can understand the sentences.A lesion in this area, 'Wernicke's aphasia', leads to being unable to produce coherent sentences - you can speak fluently but the words are nonsensical.This affects all mediums of language - audition (listening), visual (reading)
394
Outline Broca's area.
This is the region in the prefrontal cortex (frontal lobe) that is responsible for language production.This is where we produce our speech (not the language but the actual noises etc).A lesion in this area, 'Broca's aphasia', leads to being unable to produce speech (stutters/lack of words).
395
What are V2 cells responsive to?
Orientation (interstripe region)Colour (thin stripe region)
396
What can cells in V4 be responsive to and where do they pass this information to
Combinations of colour and form - pass this to inferior temporal cortex
397
Do Inferior temporal cortex cells have large or small receptive fields? and why?
They have very large receptive fields and this is so they can respond to more complex things e.g a hand shape or a face shape
398
Once an Inferior temporal cortex cell starts to respond to very complex things like a specific persons face, what doesnt affects it?
It doesnt care about the position or size of the object (or the angle at which its at)
399
What makes one object better represented in your inferior temporal lobe than another
Familiarity - the more familiar an object is, the better represeted
400
What processes the Inter-aural timing difference (ITD)
Medial superior olive (MSO)
401
What processes the Inter-aural level difference (ILD)
Lateral superior olive
402
Where are low frequency sounds processed
Medial superior olive (MSO)
403
Where are high frequency sounds processed
Lateral superior olive (LSO)
404
Which cells in the DCN mainly send information to the CNIC
fusiform cells
405
Which cells in the PVCN mainly send information to the CNIC
Octopus cells
406
Do the right hand and left hand inferior colliculus cross talk (send axons to each other)
Yes they do
407
Do the right and left sides of the medial geniculate nucleus cross talk (send axons to each other)
Yes they do
408
Outline Meissner corpuscles in terms of their afferent properties.
FA I Small sharp bordered receptive fieldsFast, no static response (action potentials at the start and end of stimulus)
409
Outline Pacinian corpuscles in terms of their afferent properties.
FA IILarge obscure bordered receptive fields.Fast, no static response (action potentials at the start and end of stimulus)
410
Outline Merkel cells/disks in terms of their afferent properties.
SA ISmall, sharp bordered receptive fields.Slow, static response present (fires due to indentation - fires while the pressure is maintained).
411
What are the names of the 4 types of mechanoreceptors from the hand? (Both names)
FA I - Meissner corpuscleFA II - Pacinian corpuscleSA I - Merkel disksSA II - ...
412
Outline the study by Johnson and Phillips (1981) into form discrimination.
Form discrimination task:The experimenter places your finger on one of two stimuli:Horizontal ridgesVertical ridgesCalled ‘gratings’The task is simply to say which orientation grating you are touching.RESULTS:= 100% correct discrimination at 2mm width between gratings.= Discrimination threshold ~ 1mm (the point at which there was 75% correct discrimination).
413
Outline the receptor density of the afferent nerve fibres of the hand.
SA-I density 100/cm^2 (1mm spacing).FA-I density 150/cm^2 (0.8mm spacing).FA-II and SA-II density lower.
414
Which neuron fibre types are best candidates for being responsible for our 1mm discrimination threshold (think Johnson and Phillips)?
Merkel type SA-I and Meisnerr type FA-I because they have a high enough receptor density to discriminate.
415
Outline the study by Phillips et al (1990) into mechanoreceptors of the hand.
Researchers used microneurography to locate a single mechanoreceptor located at the finger tip of a monkey.Then presented a barrel stimulus which had braille on it which would slowly sweep across the monkeys skin, activating the receptors sensitive to touch.This was done with the different types of receptors (SA-I, SA-II, FA-I and FA-II) to create a 'neural image' from which they would be able to tell the level of accuracy each receptor had, and therefore infer its function.RESULTS:- Neural images for SA-II and PC (in monkeys) are poor, therefore UNLIKELY to underly form perception.- SA-I type neural image was very close to real life stimulus, and FA-I were not as accurate but does convey some information to the nervous system.
416
Provide evidence that FA-II and SA-II afferents are NOT the basis of form discrimination.
Large RF'sLow spatial density on skin.Neural images of braille characters are indistinct.
417
Which type of mechanoreceptors are in part responsible for form discrimination.
SA-I and FA-I.
418
Outline the study by Maricich et al (2009) to see if Merkel (SA-I) fibres are required for form discrimination.
Hypothesis: Merkel cells are required for texture discimination - mice without merkel's should be severely hindered at this task.Experimenters used a protein marker called Keratin 8 to label all the merkel cells - which will show red if they are present.They then made conditional knock-out mice that:- Lack Merkel cells.- Lack SA-I afferents.There was no red in the neuroimaging, so no merkel cells present, and there were no SA-I afferents so definitely no merkel cells present.They made the mice's cages have half smooth surface and half rough (sand paper) and found the time spent on each type of surface by Wild Type males and females.Wild type:- Males spent about 50/50 on each surface- Females spent about twice as much time on the smooth.Knock out mice:- Females spent about 50/50 on each surface.This shows that in the mice lacking merkels, they didn't discriminate the floor surface and therefore spent equal times on both.THIS IS EVIDENCE FOR MERKELS BEING REQUIRED FOR FORM DISCRIMINATION.
419
What are the two examples that prove that Merkels are:- sufficient for form discrimination.- necessary for form discrimination.
Sufficient for form discrimination:- ElectrophysiologyNecessary for form discrimination:- Merkel-less mice.
420
What are vibrations described by?
Amplitude and frequency.
421
Outline the study by Mountcastle et al (1972) into vibration detection thresholds.
Trained monkeys/humans (primates) on discrimimating these types of vibration stimuli.A buzzer was attached to the finger, allowing the application of different vibrations.In this experiment only the amplitude changed – participants were told to say whether they could detect the vibration.RESULTS:- The 50% detection rate for amplitude was around 7 micrometres. - (this was at a certain frequency).
422
Outline/(go look at lecture 17) the graphs by Mountcastle showing the relationship between vibration frequency and its amplitude detection threshold.
Starting at low frequency, the amplitude needed to be ~100um to be detected.This decreased down to around ~200Hz as the required amplitude lowered in a steep decline.After 200Hz the required amplitude for detection then increases again.The graphs are near identical for humans and monkeys.(graph looks like a reverse Nike tick - only a small shift in positioning across species).
423
What is meant by neuronal detection threshold in reference to vibration?
The minimum amplitude amplitude that would evoke a response.
424
Outline the three possible relationships between neuronal and behavioural detection thresholds - what do they imply?
Neurons might be:- less sensitive: neuronal thresholds > behavioural thresholds (this would mean that neurons don't pick up on the vibrations before our behaviour does)- as sensitive: neuronal thresholds = behavioural thresholds (occur concurrently)- more sensitive: neuronal thresholds < behavioural thresholds (neurons detect the information before we do behaviourally - implies knowledge of neurons before our conscious awareness)
425
Outline the behavioural and neuronal data for FA-I afferents in response to vibration.(Graphs in lecture 17 - very useful to go look at these now).
Behavioural data:The solid line on this plot shows to us that the higher the frequency, the lower the threshold was for amplitude – we were more sensitive to these frequencies.The lower the frequency, the higher the amplitude needed to be to elicit a response out of us.This is true up to 200hz and then the sensitivity tails off a bit and requires higher amplitudes again.Neuronal data:The dots represent a response from an individual neuron.Their position shows the amplitude required to elicit a response at a certain frequency.Dots below the line are more sensitive then our behavioural response, dots above the lines show that they are less sensitive.The ones below the line are significant because they show that they can be more sensitive to our surroundings then our own perception is.SUMMARY:- At frequencies <30Hz, some FA-I are at least as sensitive as behaviour.- At frequencies >3Hz, FA-I are less sensitive than behaviour.
426
Outline the behavioural and neuronal data for FA-II afferents in response to vibration.(Graphs in lecture 17 - very useful to go look at these now).
See graph for data.At frequencies <30Hz, FA-II are less sensitive than behaviour.At frequencies >30Hz, Some FA-II at least as sensitive as behaviour.Showing that pacinian corpuscles are sometimes more sensitive than our behavioural perception.
427
Summarise key information about our detection of vibration.
Limits of behavioural performance (conscious perception of the vibration) is determined by individual neurons.(How sensitive we are to vibration comes from individual neurons).FA-I play role in low frequency 'flutter' detection.FA-II play role in high frequency detection.
428
Outline the study be Johansson & Westling (1984).
Precision grip test to measure the grip force used to pick up a load force.The grip force has to be >/= to the load force, or the item will slip.- acceleration shows the slip events as you grip harder quickly when you notice the slips.(Look at slide - hard to explain without diagrams and data presented).
429
What might be the natural function of FA mechanoreceptors?
Manipulation of objects.Humans excel at using tools - that is what made us, and continues to make us successful.Tool use requires vibration detection.
430
Name 3 attributes that behaviourally important body parts have.
Large magnification factorSmall receptive fields.High sensitivity (2-point discrimination test).
431
Outline the study by Merzenich et al (1984) into cortical plasticity.(One digit variation)
(See week 19 for the somatotopic maps for this study)Used electrophysiology.The numbers refer to the digits (1 is thumb, 5 is pinky).The letters refer to parts of the finger:- D = Distal, finger tip.- M = Medial, middle finger- P = Proximal, base of fingerCapital P followed by a number refers to the pads just below your fingers.Merzenich thought if you dramatically disturb the afferent information coming into the cortex, then plasticity would occur.He tested this by amputating digit 3 of the hand (professionally so the finger was removed and healed).In the old vision, they would find the same map of the monkeys hand before the removal and after – no plasticity.If there was change, then the monkey would’ve had plasticity and proved that it occurs.RESULTS:- The somatotopic map after 62 days had reorganised.- The region that used to represent digit 3, now was being used by digit 2 and 4.
432
Outline the study by Xerri et al (1994) into female rats.
Research into the difference of the somatotopic representation of ventrum (nipples) control and lactating rats.Took a somatosensory map pre birth.Once birth, one group split from litter so that they would not lactate and have stimulation of the ventrum. The other left with the litter so there is a big increase in stimulation of this area.Used electrophysiology to observe the changes.RESULTS:- Much larger representation of the ventrum in the somatosensory cortex in the lactating group.- Increase in magnification factor and decrease in RF size for the lactating group.CONCLUSIONS:- This shows that the plasticity mechanism does occur but naturally.- Showing that body maps are not static or fixed.
433
Outline the study by Merzenich et al (1984) into cortical plasticity.(Two digit variation)
Same methods as one digit variation:- Amputate fingers - this case 2- Let it heal- Remap the somatosensory cortex and see if plasticity has occurred.RESULTS:- Adjacent fingers (1 and 4) expanded their representation.- A little bit of the map is 'silent' - wasn't repurposed.Conclusions we can draw:- The more dramatic the damage, the less efficient/effective the plasticity will be at completely reusing the area.- Shows us that plasticity mechanisms are limited to some degree.
434
What is the current view on somatosensory body maps? (keep answer simple)
They are not static or fixed - can be altered via plasticity mechanisms.
435
Outline Jenkins et al (1990) study into monkeys and plasticity.
Testing the prediction that extensively stimulating a certain part of a body surface will increase the representation of that part due to plasticity.Monkeys trained to contact a rotating disk with their finger tip, therefore extensive stimulation.They trained digit 3RESULTS:- Look at lecture 19 for graphs and data.- Training increased the D3 magnification factor- Training decreased the RF size.The controls stayed the same.
436
What causes cortical maps to undergo remapping due to plasticity?
Dramatic changes in the sensory drive.
437
What is phantom limb?
The illusion that an amputated or denervated limb can still be felt.
438
What are examples of phantom limb that aren't limb?(great wording)
Phantom breast - Mastectomy Phantom genetalia - CastrationPhantom lower body - Spinal cord transection.
439
Briefly outline the afferent pathway from touch to the finger to its destination in the brain.
Touch of the finger leads to:- transduction of the mechanoreceptors in finger- afferent signals to the spinal cord- then to the brain stem- then thalamus- then region of the primary somatosensory cortex which represents the finger.
440
How does the brain know that a body part has been touched?
It infers due to which region of the somatosensory cortex is active.
441
Outline the study by Moore and Schady (2000) into phantom sensations.
Had patients with denervation of the hand.Using intraneural stimulation of the nerves that innervate the denervated region, they stimulate that nerve to see if a phantom sensation could be elicited.RESULTS:- Phantom sensations can be elicited by afferent nerve stimulation.
442
Outline the study by Davis et al (1998) into leg amputees.
This was a study on patients who had phantom pain – in attempts to alleviate the pain.The surgeons opened up the skull and placed electrodes into the VPL, specifically the ex-leg region of the thalamus.They then used microstimulation on those neurons in the VPL.RESULTS:- Phantom sensations were elicited in the amputated area.CONCLUSIONS:The Central circuits can be tricked to feel a limb is there is some external stimulation of the desired pathways.
443
Outline the case study by Ramachandran et al (1992) into patient VQ.
VQ was a left arm amputee who had phantom sensations in his missing left arm.The researchers discovered that when they touched VQ on the cheek while he was blindfolded.- He felt it on the cheek, and on the thumb (region T elicited this) – the phantom thumb.- P region elicited the phantom feeling of his pinky.- Etc for the other letters - (refer to lecture 19 for pictures)The discovery was that there was a map of VQ’s phantom hand on his face - this is called a referred sensation.
444
Outline the study by Pons et al (1991) into limb deafferentation.
They used monkeys and removed the afferent drive to the brain by cutting the nerves of the arm before they enter the spinal cord.The effect of this was to disconnect the mechanoreceptors in the arm from the spinal cord.They then re-tested the monkeys 12 years later to see the plasticity that had occurred.RESULTS:- In zone 1 and zone 6 they found the receptive fields as expected for the trunk and face.- In the deafferented zone, which normally represents the arm and hand, they found the receptive fields on the face (chin to be exact)CONCLUSION:- They found a large remapping of S1 for the deafferented zone to now represent the face.- Monkeys are very similar in this neural mechanisms to humans, therefore it is likely to assume this mechanism occurred in VQ (patient).
445
Define multisensory integration at the neuronal level
“a statistically significant difference between the number of impulses evoked by a crossmodal combination of stimuli and the number evoked by the most effective of these stimuli individually” (Stein & Stanford, 2008)
446
What are the two overarching results of multisensory integration?
Enhancement (increased firing)Depression (reduced firing)
447
Why is it important to consider multisensory integration?
Many situations involve bombardment of the sensesCombining information across senses can more quickly and accurately inform us about the outside world
448
What are the three types of multisensory integration?
SuperadditiveAdditiveSubadditive
449
What is superadditive MSI?
When the MSI firing is more than either of the stimuli alone (enhancement)
450
What is additive MSI?
When the MSI firing is equal to the sum of the unisensory firing.
451
What is subadditive MSI?
When the MSI firing is lower than each of the firing alone (depression)
452
Outline the superior colliculus.
Midbrain structureHas inputs from the visual pathway.Involved in orienting behaviour:- Visual stimuli- Auditory stimuli- Somatosensory stimuliE.g., turning our head in the direction of said stimuli.
453
Outline research into MSI in the cat superior colliculus.
Recordings taken from single neurones in the Cat SC.Cells respond to both visual and auditory alone.Responded +1207% more to the combination of both stimuli which shows superadditive MSI.
454
Outline the inputs to the superior colliculus.
Sensory information from eyes and ears.Top-down information from the cortical areas (feedback).
455
Name the three principles of multisensory integration.
Inverse effectivenessTemporal ruleSpatial rule
456
What is meant by inverse effectiveness? (MSI)
Strongest effect when individual cues are weak.
457
What is meant by the temporal rule? (MSI)
Strongest firing when stimuli occur at the same/similar point in time.
458
What is meant by the spatial rule? (MSI)
Strongest firing when receptive fields overlap - i.e., the stimuli received by each sensory modality come from the same spatial area (seeing a dog, hearing it bark - both come from the physical position of dog. If the bark was behind and the dog was in front, the signal would be less)
459
Briefly outline the study into multisensory receptive fields in cats (Stein et al., 2020).
Measured the cat superior colliculus.Used a semi circle of speakers and screens to independently manipulate the location of auditory and visual stimuli.Found that overlapping receptive fields from two modalities had the largest response.Animals can orient rapidly to location of the stimuli (SC does this).
460
Briefly outline the findings of the study into visuo-tactile receptive fields in monkeys (Graziano et al.).
Visual and tactile receptive fields are spatially aligned. (If you see a stimulus approaching your face, you associate it with the sensation of that area of your face - building up connection between visual and tactile perception).Visual RFs restricted to area surrounding the body - peripersonal space (your personal bubble)Visual RFs are anchored to body parts too (some will be anchored to your hand - fly landing will be felt if you look, won't if you don't)Reduced response found as visual stimulus moves further from the body.
461
Briefly outline the study into remapping of RFs in monkeys (Graziano & Gross).
Measured from cells in the primate ventral pre-motor cortex.Found that visuo-tactile RFs update with changes in body position and fixation(see lecture on MSI for pictures)When right arm was out, there was the strongest response to stimuli close to the right arm.When the left arm was out, the strongest response shifted to the left closer to the arm that was out.
462
Name 3 ways that speech perception can be impacted by visual information.
Improve perception: seeing lip movements in noisy area.Influence WHERE in space we perceive a sound source (ventriloquism).Change what we hear: McGurk effect
463
Outline the McGurk effect.
A noise such as 'ba-ba' being heard, can be changed by changing the visual input.If the same 'ba-ba' stimulus is played, yet a video shows the person saying 'fa-fa' then you will perceive 'fa-fa'
464
Eating is a multisensory experience, give 3 examples of how our experience of food can be changed via changes to the sensory experience.
Artistic presentations of food make people perceive it as tastier.Foods taste crunchier and fresher when the sound is amplified or the high frequencies increased (Spence and colleagues)White noise can diminish ratings of taste intensity (Woods et al., 2010)
465
What is the parchment skin illusion?
Our hands feel drier when the volume/frequency of rubbing them is increased (because the noise is associated with dryness).
466
Name the 4 modalities of sensory reception and their associated receptor type/
Mechanical - mechanoreceptorThermal - thermoreceptorChemical - chemoreceptorElectromagnetic - photoreceptor
467
What are the two main types of skin?
Glabrous (smooth)Hairy (Back of hands/legs)
468
What is sensory transduction?
Conversion of physical energy to a receptor potential in a receptor neuron.
469
Name the receptor cell types in the skin. (5)
Merkel cellsRuffini endingMeissner corpusclePacinian's corpuscleFree nerve endings
470
What is sensory coding?
The neural representation of stimulus energy in terms of action potentials.
471
What is the relationship between action potentials, receptor potentials and stimulus strength?
They are proportional:The stimulus strength increases the intensity of the receptor potential.And then action potentials firing rate is proportional to this - if there is a large receptor potential (high strength of stimulus), then there will be a faster rate of firing of AP's(Lecture 16 for pictures)
472
Why is the C elegans (nematode) used in research into sensory transduction?
It's a worm, that isn't usually green - but can be genetically engineered to express the GFP in its neurons.(GFP - green fluorescent protein)There are parts of the worm that are so intensely green they appear white, as there is a denser concentration of neurons (shows area of nervous system).As there are only 300 total neurons, you can oblate and precisely kill one cell and try to work what the role of that cell was in the animal.
473
Outline research into C elegans (nematode) and its sensory system.
Which neurons in the nematode are involved in the reaction to touch?METHOD:Systematically oblate the GFP labelled neurons between experimental conditions.Then, gently prod the animal in parts to see its behaviour.- Touch its tail, swims away.- Touch its head and it goes other way.As you oblate different neurons, once there isn't a reaction to touch, you can identify which neurons are responsible for which part of its sensory system.RESULTS:PLML and PLMR are motor or sensory neurons in the tail.(I don't think rest are important - check lecture 16 for picture)
474
Outline the study (O'Hagan et al., 2004) into determining whether neurons are sensory or motor neurons in the C elegans (nematode).
METHODS:- GFP labelling of PLM cell - so we can see where to record from under fluorescent microscope.- Record from the cell via electrophysiological recording.- Carefully touch animal and see the response.- Record the response.**If there is receptor potential, then it shows they are sensory neurons - not motor.**RESULTS:- There was a receptor potential, therefore they are sensory neurons.- The latency between prodding and receptor potential was very small, suggesting that the mechanical stimulus is directly impacting the opening of the ion channels.
475
Outline the study (Coste et al., 2010) into finding the molecular basis of somatosensory transduction. (2 steps)| (HINT - P..... 1 discovery)
METHODS: *Step 1*- Cell line is an immortalised cell that can grow in a culture in the lab, ideal for research.- First, need to find cell line that they could use to model mechanotransduction: needs to respond with a receptor potential in response to being touched.- They found one! (using a 'poke' assay)- They used a blunt probe and found that the bigger the poke, the bigger the response (therefore mechanically activated current)- Used whole cell electrophysiology to measure the current through the membrane in response to being poked.-------------------------------Next step is trying to figure out what genes/proteins are involved.-------------------------------METHODS: *Step 2*- Did DNA microarray to identify proteins and genes involved.- Restricted search to that of genes relating to proteins in membrane.- Then systematically interfered with function of genes using small interfering RNA (siRNA knockdown).- For each interfered with gene, checked if a RP was exhibited:- If so, gene not significant, *if not* gene plays MAJOR role in RP being exhibited.RESULTS:- *the only gene that showed significance for inhibiting the occurrence of a receptor potential post poke was Piezo 1 gene.*
476
Outline Piezo 1's role in understanding somatosensory transduction.
It was found in the Coste et al. 2010 study as a significant gene for this process (fucking w this gene stopped RP's occuring in response to touch).However, it might not be expressed in somatosensory neurons - it's found in knee joints, blood vessels and kidneys etc.Found another gene with similar structure, **Piezo 2** - which IS expressed in sensory neurons.*But this doesn't show it is required - only present (further testing needed*SO basically - seems like it was important in finding Piezo 2 (more on that in other flashcards) which still needed to be studied:- Piezo 1 seems to be the stepping stone to finding the answer.
477
Outline the studies (Coste et al., 2010, Ranade et al., 2014) into Piezo 2 as an explanation for somatosensory transduction.
METHODS: (Coste et al)- They performed a heterologous expression of Piezo 2 in cell lines (didn't occur naturally).- Then asked - will a receptor potential be elicited? - if so, then it was key to somatosensory transduction.RESULTS: - They did see a receptor potential if Piezo 2 was in the cell.- Therefore, **it is** sufficient for transduction to occur.- Just because it is sufficient, doens't mean it is how transduction works under normal circumstances...METHODS: (Ranade et al)- Did a behavioural test on Piezo 2 knock-out mice.- Hypothesised that the mouse would have a reduced tendency to run away due to touch if the gene was knocked out.RESULTS:- Found **significant** difference in response to poking between WT and Piezo 2 knock-out mice - thus proving its role in transduction.- (Much smaller response in knock-out mice - Normally the mice respond 70% of the time, without Piezo2 there was only 15%)
478
Outline the study (Lam et al., 2023) into Piezo 2 and sexual function. What was the key idea behind the research?
Where researching to find the generality of the role of Piezo2 in touch - it should be involved in sexual behaviour if it is the key to somatosensory transduction.METHODS:- Used a test of touch sensitivity: von Frey hairs (plastic apparatus that allows for precise force application.- Used Piezo knock-out mice (Piezo2^Hoxb8).- Tested response to genital touch (IV1) AND succesful mating behaviour (IV2)RESULTS:- **IV1**: Found that the knock-out mouse in the genital condition shows that they became a lot less sensitive (strong force required to generate response compared to the small 500ug required in WT).- **IV2**: WT had 70% succesful homozygous mating, whereas knockout x WT mating was between 0-10% succesful.AGAIN shows the involvement of of Piezo 2 in touch.
479
What is meant by heterologous expression in reference to genetic enginering?
Refers to the expression of a gene or part of a gene in a host organism that does not naturally have the gene or gene fragment in question.(Insertion of the gene in the heterologous host is performed by recombinant DNA technology)
480
How do action potentials generated by mechanoreceptors reach the CNS?
Via the axons:Stimulus -> receptor potential -> axons -> spinal cord
481
What does 'primary afferent fibres' refer to?
Sensory axons - they connect the peripheral branch of the nervous system to the central branch.
482
Where are the somas of the body's primary afferents located?
Just outside the spinal cord in the dorsal root ganglion cells.
483
Where are the somas of the face's primary afferents located?
Just outside the spinal cord in the trigeminal ganglion cells.
484
Outline the structure of somas (cell bodies) of axons in relation to how they connect to the peripheray and central branches of the nervous sytem.
Somas don't have any dendrites - they have one primary axon that splits in two:- One branch goes to the PNS.- One branch goes to the CNS.The flow of information is determined by whether they are afferent or efferent:- Afferent = away from periphery towards the CNS- Efferent = away from the CNS towards the periphery
485
What are the two main types of primary afferents, and what is the cause of this difference?
Thick = myelinatedThin = unmyelinatedThe more myelination, the thicker the axon - their size is different depending on their location within the body.
486
What are the 4 subtypes of primary afferents? What is their characteristic difference?
C fibres = no myelin at allA alpha fibres = Lots of myelinA beta fibres = medium amount of myelinA delta fibres = small amount of myelinThey each have different roles.
487
Outline the study (Adrian & Zotterman, 1926) into the different types of nerve fibres.
These were the pioneering experiments that found out different neurons had different properties.METHODS:- Used electrophysiological recording (1926 so did this by getting the tip of a wire really close to neurons - this allowed them to measure them).- They did a poke test to see what each neuron type would respond to.RESULTS:- Neurons that would respond to gentle touch were **low threshold mechanorecptors**- Neurons that only responded to harmful or potentially harmful stimulus were **high threshold mechanoreceptors** (nociceptive)- Neurons that responded to changes to temperature were **thermoreceptors**.
488
What do low threshold mechanoreceptors respond to, and what fibre type(s) are associated?
Gentle touch, Aalpha fibres and Abeta fibres
489
What do high threshold mechanoreceptors respond to, and what fibre type(s) are associated?
Only respond to harmful/near harmful stimuli (nociceptive) - Adelta and C fibres
490
What do thermoreceptive neurons respond to, and what fibre type(s) are associated?
Changes in temperature (hot/cold) - Adelta and C fibres
491
Outline the paradoxical relationship between fibre type, their role, and their characteristics.
Aalpha and Abeta:- Have lots of myelin and are thick, therefore very fast transmission of information.- Responible for relaying info about gentle touch.Adelta and C fibres:- Are unmyelinated/have little myelin and are thin, therefore slower transmission of information.- Responsible for relaying nociceptive signals.**Pain information reaches the brain slower than gentle touch.**
492
Where are cutaneous low-threshold mechanoreceptors found? What is the acronym for them?
(LTMRs) - found in glabrous skin (smooth)
493
What is meant by the receptive field of a fibre/neuron?
The area of skin to which stimulation of increases the firing rate of said neuron.
494
Outline the experiment into the response of different neuron types due to touch to the skin.
METHODS:- Indent the skin for 2 seconds, then release.- Use electrophysiological recording to identify the firing rates of different neuron types.RESULTS:- Slow adapting neurons fire the whole time the stimulus is applied for.- Rapidly adapting neurons fire ONLY at the onset and offset of the stimulus.
495
Outline the classification of neuronal fibre types in relation to firing rate and receptive field size.| You will have seen this in a table.
FA fibres = means fast adapting - fire only at the onset and offset of a stimulus.SA fibres = means slow adapting - fire throughout the whole presentation of the stimulus.Type I = means small receptive fields.Type II = means large receptive fields.Therefore:FA-I :- Fast adapting, small receptive fields.FA-II:- Fast adapting, large receptive fields.SA-I:- Slow adapting, small receptive fields.SA-II:- Slow adapting, large receptive fields.
496
Outline the comparative terminology for monkey nerve fibres in comparison to human terminology.| (Fibre type names based on firing characteristics and receptive fields)
Layout: Human : MonkeyFA-I = RA or QASA-I = SAFA-II = PCSA-II = (no equivalent found yet)
497
Outline the position of the receptor cells in skin in relation to their depth.
Meissner corpuscles and Merkel discs: - Have superficial (near the surface of the skin) nerve endings (small RF's)Pacician corpuscles:- Have deep nerve endings (large RFs)
498
Outline the key basic information about Merkel discs.
MOST COMMON!Axon sheds myelin and innovates merkel disk as it gets close to it Have small receptive fieldsSlowly adapting **SA I Type**100 per cm^2 in hand (high concentration in fingertip)
499
Outline the key basic information about Meissners corpuscles.
Encapsulated by concentric schwann cellsHas a schwann cell laminaeHave small receptive fields Are rapidly adapting - good at detecting change**FA I type**150 per cm^2 (in fingertip)
