Senses (Hearing, Vision, Olfaction, Gustation) Flashcards

1
Q

Detail 4 problems affecting refraction potential in the lens. How are they mitigated?

A

Chromatic aberration: red light has lower refractive index than blue, so dispersion of λs on retina.
- Retina has yellow pigment over fovea and fewer blue cones to compensate for more blue light refracted into centre.

Spherical aberration: edges of lens bends light eccentrically
- Cornea is ellipsoid
- Refractive index of lens is lower at edges

Glare: light scatters in cornea
- Reduced by choroid

Diffraction: light scattered by restricted aperture
- Pupil can change size according to light intensity

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2
Q

What is the point spread function?

A

A way to quantify blur caused by the optical system.

Tested for using grating patterns - smallest grating that is still distinguishable at given contrast.

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3
Q

What consequence does convergence have in the retina?

A

No 1:1 mapping as huge convergence for receptive fields.

75,000 rods to 5000 bipolar cells converge to 1 ganglion cell.

Density is roughly 1 receptor every 2-3µm

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4
Q

How is pupil size controlled? What are the consequences of different sizes of pupil?

A

Dilation:
- Sympathetic nervous system control of radial dilator muscles
- Receives more light and minimises diffraction
- Decreases depth of field

Constriction:
- Parasympathetic control from Edinger-Westphal nucleus in brainstem to ciliary ganglion.
- Increases depth of field and minimises aberrations
- Increases diffraction and reduces light intake.

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5
Q

Give some ways that the eye is adapted to cope with a large range of photon intensities (range of 10^12)

A

Pupil diameter: copes with roughly 1 order of magnitude

Types of receptor:
- Photopic vision (cones) at high illumination
- Mesopic vision (both rods and cones)
- Scotopic vision (rods) at low illumination

Adaptation of each receptor type:
- Rods have slower adaptation (30mins)

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6
Q

What is a Purkinje shift and what does it show?

A

A shift in peak colour sensitivity at lower light intensities to shorter wavelengths

Gives evidence for different cell populations, since lower light intensities utilise more peripheral retina which has higher S cone density.

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7
Q

Describe the behaviour of a centre red; surround green receptive field.

A

ON centre for red; ON surround for green
- Red light on centre and green light on surround causes maximum firing (both areas depolarise bipolar cell as sign reversing)
- Red light over whole area causes weak firing
- Green light over whole area means bipolar cell does not fire
- Green centre; red surround means cell inhibited from firing (maximum hyperpolarisation of bipolar cell)

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8
Q

Describe the difference between and distribution of RGN for the magno and parvo pathways:

A

M pathway: Parasol cells with a larger receptive field

P pathway: midget cells with smaller receptive field.

In peripheral retina: roughly 50/50 distribution. In centre: 90% midget cells (higher spatial acuity)

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9
Q

Compare and contrast midget and parasol cells:

A

Parasol cells (5% of ganglion cells):
- Includes ON and OFF types
- Faster and more transient responses (faster adapting)
- More sensitive to low-contrast stimuli

Midget cells (90% of ganglion cells):
- Includes both ON and OFF
- Slower and more sustained responses (can deal with higher contrast)
- Can be colour opponent ganglion cells

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10
Q

How is light energy transformed into an electrical signal?

A
  1. Rhodopsin/iodopsin in outer disc segments absorbs photons
  2. Retinal molecule in the opsin changes conformation activating a Gtransducin coupled receptor
  3. PDE activated which degrades cGMP
  4. Results in closure of cGMP gated Na+ channels
  5. Hyperpolarises cell, and resuces internal Ca2+, reducing glutamate release
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11
Q

How is retinal recycled in retina?

A

Unstable metaopsins will split within minutes – trans retinal released to be converted back to cis
- Trans retinal transported to epithelial cells
- Reduced to all-trans retinol (= vitamin A)
- Converted back to cis retinal to be transported back

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12
Q

How is a photoreceptor returned to a dark state?

A

Goal is to increase Ca2+ levels

Transducin modulated mechanisms:
- Phosphorylation of metarhodopsin leads to arrestin activation = stops transducin activating PDE
- Transducin has intrinsic GTPase activity

Drop in intracellular Ca2+ has -ve feedback effect upregulating recovery speed:
- Increases guanylate cyclase activity to restore cGMP levels
- Upregulate arrestin levels as recoverin is activated
- Increases Na+ channel affinity for cGMP

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13
Q

How does a drop in intracellular Ca2+ (caused by light) oppose further hyperpolarisation?

A
  • Recoverin activity increases, increasing rhodopsin phosphorylation and reducing transducin activity.
  • Accelerates guanylate cyclase activity
  • Increases channel affinity for cGMP using Ca-CAM
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14
Q

How do different bipolar cells show sustained vs. transient responses?

A

Sustained response:
- b3/b7 cells express lots of kainite receptors
- Results in tonic response

Transient response:
- b2 cells express high AMPA density
- Phasic stimulation (higher frequency)

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15
Q

Describe the route of neurons from the retina to V1:

A

Optic nerve
Optic chiasm
Optic tract
Lateral Geniculate Nucleus (Thalamus)
— Small number to hypothalamus and superior colliculus) —
Optic radiations
Brodmann’s area V1

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16
Q

Describe the organisation of visual information the LGN

A

Layered organisation:
- Parasol cells input into magnocellular neurons (M pathway) to layers 1&2
- Midget cells input into parvocellular neurons (P pathway) layers 3-6.
- In between layers input from koniocellular neurons giving colour information (mainly blue-yellow)

Layers 1,4,6 are from contralateral eye and layers 2,3,5 are from ipsilateral eye so same areas of visual field are kept together.

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17
Q

Describe how the retinotopic map in V1 is organised:

A

Layers:
- Six layers
- Koniocellular into II and III
- IVCα: mainly magnocellular neurons
- IVCβ: parvocellular neurons

Columns:
- Each area corresponds to area in visual field.
- Horizontal connections but mainly ocular dominance (each IVC neuron receives input from one eye)
- Determines orientation preference

Rows:
- Blobs (centered on ocular dominance stripe) and interblobs
- Blobs receive input from M pathway, P-B sub-pathway and koniocellular cells.
- Interblobs receive information from P-I sub-pathway (direction selectivity) and M pathway

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18
Q

What information do blobs and interblobs process?

A

Interblobs: shape processing
- Direction selectivity
- input from P-I pathway and M

Blobs: movement and colour
- Colour processing (yellow-blue from koniocellular and red-green from P-B)

Both interblobs and blobs combine information with columnar info on orientation (simple, complex and hypercomplex cells)

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19
Q

What is the difference between the P and M pathways?

A

P-pathway is important for high spatial acuity and colour vision

While the M-pathway is important for high visual sensitivity and motion vision

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20
Q

Give examples of higher level processing:

A
  • Composite shape response (e.g. corners)
  • Disparity (depth perception)
  • Border ownership signals (is something foreground or background?)
  • Contextual information (e.g. fill in scotoma (blind spot) using surrounding area
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21
Q

What is the ventral stream for vision?

A

The ‘What’ pathway:
- Receives information from P pathway: blob (colour) and interblob (shape)
- Sensitive to complex shapes (e.g. curvature)
- Show lighting; colour and size consistency

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22
Q

What does V4 connect to for higher level processing?

A
  • Parahippocampus: memory recall of objects
  • Pre-frontal cortex for decision making
  • Temporal lobe for learning and memory
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23
Q

What is visual agnosia? What types are there?

A

Abolished ability to recognise objects while vision remains good = the ventral stream gone wrong.

Apperceptive agnosia: Can recognise objects but not copy them

Associative agnosia: can copy objects but not identify them.

Specific damage can cause other effects e.g. prosopagnosia (type of associative) with inability to recognise faces.

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24
Q

What is the dorsal stream? What is the evidence for this being separate from the ventral stream?

A

The ‘Where’ pathway.

Balint’s syndrome suggests different streams:
- Preserved recognition but impaired eye movements and reaching toward objects.
- Shown by posting experiments

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25
Q

What are the purposes of the outer ear?

A

Amplification:
- Ear canal causes resonance particularly to 2-5Hz (useful for human speech)

Localisation:
- Head related related transfer function creates characteristic notches in wave function depending on position.

26
Q

What is the evidence for the plasticity of interpretation of sound waves entering the pinna?

A

Interpretation of HRTF is plastic and can be re-trained
- Shown by experiments where pinna are blocked.
- Initially localisation accuracy collapses
- Improves over weeks
- After block removal; accuracy is still good

27
Q

What are the functions of the middle ear?

A

Impedance matching:
- Amplification: match air borne sound wave with fluid filled ear

Protection:
- From damagingly loud sound
- Echo reduction (from spongy structure)

Anti-masking:
- Lower frequency sounds are masked by higher Hz. THerefore lower Hz amplified more.
- Partly achieved by middle ear muscles

28
Q

How does the middle ear achieve impedance matching?

A
  • Match air borne sound wave with fluid filled ear
  • Achieved by area ratio of tympanic membrane to magnify sounds
  • Improved by lever action of malleus and incus bones
29
Q

What are the functions of the middle ear muscles?

A
  • Protection from self sounds: contract 100ms after exposure and before a person vocalises (absent in frogs which do not vocalise suggest self-protection mechanism)
  • Attenuate low frequencies more
  • Reflex circuit links both ears together (even if only one stimulated – protection)
30
Q

How is mechanical movement of air transferred to electrical potentials?

A
  1. Staples vibrates oval window causing vibrations to the incompressible fluid
  2. Basement membrane vibrates
  3. Causes movement of fluid into/out of organ of Corti
  4. Displaces IHC stereocilia
    - Towards longest hair = excitation
    - Towards shortest hair = hyperpolarisation
  5. Depolarised IHCs open VG Ca2+ channels causing glutamate release onto AMPA receptors
31
Q

How is the movement of stereocilia linked to the potential state of an IHC?

A
  • Movement of fluid causes stereocilia movement
  • Displacement towards longest cilia stretches tip links
  • Opens outward K+ channels
  • Depolarises cell
  • Opens VG Ca2+ channels
  • Glutamate released onto AMPA receptors on auditory nerve
32
Q

What are the roles of OHCs?

A

Attached to both techtorial and BM

Amplifies vibration at specific point on BM:
- Compliance increases on stretching and decreases on compression giving +ve feedback

Modulation:
- Hyperpolarisation causes length increase; depolarisation causes decrease
- Top down control from olivocochlear nucleus
- Results in adaptation, sensitivity and sharpening of hearing
- Antimasking properties

33
Q

How is a tonotopic map created by the basilar membrane (BM)?

A
  • Narrower and stiffer at base
  • Therefore resonant to higher frequencies at base and lower at apex
  • Creates logarithmic map of frequencies per distance along membrane (more distinction for higher Hz)
  • Allows for place code to function to determine frequency
  • Effectively creates a band pass filter due to large change in threshold sensitivity.
34
Q

What are oto-acoustic emissions and why are they useful?

A
  • Sound waves produced by the ear due to colliding vibrations from incoming frequencies on the BM
  • People with sonsorineuronal hearing loss lack OAE therefore used for neo-natal diagnosis.
35
Q

What is the effect of spontaneous discharge rate in auditory cells?

A
  • Lowest threshold cells are highest sensitivity but saturate at lowest dB of sound
36
Q

What is the function of the round window and stria vascularis?

A

Round window: relieves pressure when volume of organ of corti changes.

Stria vascularis: controls the [K+] in endolymph
- Must be kept high as K+ current allows IHC depolarisation
- K+ transported by active transport

37
Q

What is the duplex theory of sound localisation?

A

Interaural time differences (ITDs) used for lower Hz

Interaural intensity differences (IIDs) used for higher Hz

38
Q

What are the mechanisms by which frequency of sound is determined?

A
  • Phase locking for periodicity coding
  • Place coding: tonotopic map of the basilar membrane
39
Q

Explain how phase locking codes frequencies of sound.

A

Low frequency auditory neurons discharge at a specific point on the phase of a sound wave:
- May not discharge for every cycle
- Over population; can code high frequencies (repolarisation time for one cell is compensated for by population)
- Up to 8000Hz in Barn owl
- At high frequencies there is sustained depolarisation over which frequency is overlaid (reduces repolarisation time)

40
Q

How are ITD and IID used?

A

Used to help with sound localisation

ITDs: phase difference between ears suggests where sound is coming from.
- Detectability range is 10µs to 660µs
- Phase difference ambiguous at high Hz where diffraction around head impaired.
- Decoded by Held (monster) synapses in OC

IID: sound from one side is shielded by head
- More different at high frequencies where diffraction impaired

41
Q

Give some adaptations of the barn owl which give it highly sensitive hearing:

A
  • Acoustic fovea where localisation is most accurate
  • Ears at different heights

Very fine ITD and IID resolution:
- ITD: nucleus magno-cellularis neurons respond to tone pips with narrow dynamic ranges
- IID: nucleus angularis neurons have wide dynamic ranges

42
Q

How does coincidence detection work in the Barn owl?

A
  1. Nucleus Laminaris receives information from bilateral magnocellularis nuclei
  2. Neurons are organised in a ladder formation and fire when stimuli arrive simultaneously
  3. Have a set on both sides to give two planes of information
  4. Each neuron is sensitive to a specific time disparity (given by its position) depending on its distance down the ladder
43
Q

How is spatial sound information organised in the barn owl?

A

A space map is formed using ITDs and IIDs

44
Q

How does the barn owl use IIDs?

A
  • Inhibitory stimuli from the ipsilateral side and excitatory signals from the contralateral side (balance of these signals determines output)
  • Bottom of lemniscal nucleus has ipsilateral stimulated neurons while top has contralateral stimulated neurons
  • Due to distribution the output only responds to positive intensity differences i.e. when sound is further from ipsilateral side.
45
Q

How do odorants reach the olfactory receptors?

A
  • Dissolved into mucus film
  • Receptors distributed into 4 zones
  • Turbinates enlarge olfactory epithelium in some rodents

Pheromones detected by vomeronasal organ detects pheromones.

46
Q

How are distributions of olfactory receptors shown experimentally?

A
  • Adenovirus vector – contains odour gene and GFP used to infect receptors
  • Fluoresce to ensure it has been taken up
47
Q

Describe the transduction pathway in receptors:

A
  • Odorant interacts with receptor activating GolfPCR
  • Stimulates adenylyl cyclase to produce cAMP
  • cAMP opens nucleotide gated cation channels
  • Inward flowing receptor current (carried by Ca2+ and Na+)
  • Effect amplified by outward Cl- flow through Ca2+ gated anion channels
  • Cl- actively accumulated by NKCC2 pump
48
Q

How are changes in odorant concentration and duration conveyed?

A

Concentration:
- Receptor current rises with increased odour concentration
- Gives graded elevation in spike firing rate

Duration:
- Receptor current oscillations showing coupled changes in Ca2+ and cyclic nucleotide concentrations suggest continued stimulation
- While preserving spike coding

49
Q

What adaptation mechanisms exist for the olfactory system?

A

Transduction in receptor:
- Calmodulin-Ca2+ acts to reduce the sensitivity of cation channels to cAMP

Lateral inhibition from mitral and granule cells

50
Q

Describe the route of olfactory information from receptor to glomerulus:

A
  1. Receptor
  2. Axon of receptor to olfactory bulb (passing cribriform plate)
  3. Synapses mitral cells which interact with granule, tufted and periglomerular cells to facilitate lateral inhibition
  4. All receptors of same type meet at their olfactory glomerulus
51
Q

Describe lateral inhibition between olfactory receptors:

A
  • Mediated by periglomerular and granule cells
  • Form reciprocal dendro-dendritic synapses creating ‘curtain of inhibition’
  • Reduces noise and sharpens odour tuning
  • Mitral cells inhibit their contralateral bulb
52
Q

What is the combinatorial code of olfaction and how is it tested experimentally?

A

The pattern of glomeruli activation giving identity to the molecule.

Experimentally tested:
- Expose olfactory epithelium to mild detergent and labelled pseudorabies virus
- Expose to smell
- Optically see which cells respond in olfactory bulb

53
Q

What is the limbic system? How does it link to olfaction?

A

A collection of brain structures dealing with emotion, memory and arousal

Higher odour processing:
- Pyriform cortex = arousal
- Amygdala = autonomic control

54
Q

How are gustatory receptors organised and what do they connect to?

A
  • Clustered together in papillae (taste buds)
  • Synapse with afferent fibres to chorda tympani and glossopharyngeal nerve (CNIX)
55
Q

Describe the transduction mechanism for Sweet and Umami reception:

A

Heterodimeric Gq protein receptor
- Sweet: Tas1R2 + Tas1R3
- Umami: Tas1R1 + Tas1R3

Stimulates action potential (IP3)
- Opens TRP5M Ca2+ channel
- Depolarisation of receptor releasing ATP from gap-junction hemichannel

Non-vesicular release!

56
Q

Describe the transduction mechanism for bitter reception:

A
  • Sensed by TasR2 receptors
  • Around 30 in family (not all expressed by each receptor) – bitter = danger signal
  • Stimulates Gq receptor (Ca2+)
  • Depolarisation of receptor releasing ATP from gap-junction hemichannel

Non-vesicular release!

57
Q

Describe the transduction mechanism for sour reception:

A

Sour = intracellular acidification by weak acid
- Undissociated acid diffuses in (acids with higher pKa values = weaker acids acidify inside cell MORE)
- Potassium channel blocked by protons leading to depolarisation and then Ca2+ release
- Vesicular transmitter release (serotonin)

58
Q

Describe how salt is detected on the tongue.

A
  • Entry of Na+ ions through epithelial Na leak channels (ENaC) depolarises cell
  • Releases ATP as neurotransmitter through CALHM1/3 channels
59
Q

Describe somatosensory ‘taste’ receptors:

A
  • Hot chilli: capsaicin receptor TRPV1
  • Cold mint: menthol receptor TRPM8
  • Mustard oil/wasabi: noxious cold receptor TRPA1
60
Q

What are the three theories of taste coding?

A

Absolute theory:
- Labelled line coding with no overlap (disproved)

Relative preference theory:
- Individual fibres respond to a range of stimuli but prefer one
- Across fibre code: taste identified by the pattern of afferent activity evoked
- Gives concentration and molecular information

Local processing:
- Autofeedback: excitation of pre-synaptic receptor cells causes 5HT (and some ACh) release – excites afferent fibres and inhibits receptor cells
- Inhibits neighbouring receptor cells