Bio and Neuro psychology Flashcards

(341 cards)

1
Q

What is biological psychology?

A

study of physiological, evolutionary and developmental mechanisms of behavior and experience

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2
Q

What is the mind body problem? And what are the main two beliefs?

A

Mind body problem: how conscious mind and physical body interact

Monism: Mind and body are the same

Dualism: Mind and body are two different entities

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3
Q

What are the 4 types of explanations used in biological psychology?

A
  1. Physiological
    • behavior to the activity of the brain and other organs
  2. Ontogenetic (gr. origin)
    • How something develops
  3. Evolutionary
    • evolutionary history of a structure or behavior
  4. Functional explanation
    • Why a structure or behavior evolved as it did
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4
Q

What is a neuron?

A

Cell that receive and transmit information to other cells

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5
Q

What is the general structure of a neuron?

A

Nucleus, Some/Cellbody, Dendrite, Axon

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6
Q

What is the nucleus of a cell?

A

structure that contains chromosome

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7
Q

What is ribosomes?

A

structure in cells that syntheseize new protein molecules
- some float freely in a cell
- Others attached to endoplasmic reticulum - network of thin tubes that transport newly synthesized proteins to other locations

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8
Q

What is the mitochondrion of a cell?

A

performs metabolic activities - provide energy that cell uses for all activities

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9
Q

What is a motor neuron?

A

Receives excitation through its dendrites and conducts impulses along its axon to a muscle
- soma/cell body in the spinal cord

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10
Q

What is a sensory neuron?

A

Specialized at one end to be highly sensitive to particular type of stimulation

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11
Q

What are dendrites

A

Receive information from other neurons
- branching fibers that get narrower near their ends
- contain dendritic spines - short outgrowths that increase surface area available for synapses

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12
Q

What is the cell body/soma?

A

contains the nucleus, chromosomes, and mitochondrion

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13
Q

What is the axon?

A

Conveys an impulse to other neurons

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14
Q

What is a myylein sheath?

A

protective layer over axon - helps speed up transmission of impulse

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15
Q

What are nodes of Ranvier?

A

nodes of the axon that do not have a myelin sheath

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16
Q

What is presynaptic terminal/end bulb/ bouton?

A

point that axon releases chemicals that cross to another cell

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17
Q

What does afferent mean?

A

Bring information into a structure
- every sensory neuron is an afferent to the nervous system

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18
Q

What does efferent mean?

A

Bring information away from structure
- every motor neuron is efferent from nervous system

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19
Q

What is an interneuron or intrinsic neuron?

A

when a cell’s dendrites and axon are entirely contained within a structure

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20
Q

What is are the types of gila cells?

A

astrocytes: synchronize activity of a group of neurons - important in generating rhythms e.g. rhythm of breathing
Microgila: remove dead cells and weak synapses + neurotransmitter + virus
Oligodendrocytes (in brain + spinal cord) + Shcwaan cells (in periphery of body): build myelin sheaths
Radial gila: guide the migration of neurons and their axons and dendrites during embryonic development

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21
Q

What is the blood brain barrier?

A

Excludes chemicals from entering the vertebrate brain

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22
Q

Why do we need a blood brain barrier

A

Unlike other cells, vertebrate brain cannot replace damaged neurons = you can’t sacrifice neurons = gotta protect this from any virus (Protection of CNS + regulate brain metabolism)
- BUT this barrier keeps basically almost all chemicals out including useful ones –> can’t have it in the whole body as the other chemicals are needed for the other parts (con)

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23
Q

What is glucose?

A

Energy source that vertebrate brain cells depend on

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24
Q

What is vitamin B, thiamine?

A

-allow body to use glucose
- deficiency of vitamin B/thiamine -> common in chronic alcoholism, leads to death of neurons -> memory impairments

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25
What is resting potential of a neuron?
the difference in voltage between the inside and outside of a neuron (-70mV)
26
So why can't we allow any ions to pass thru the membrane of the neuron?
Neuron is covered by membrane, sandwiched in the middle of two layers of phospholipid molecules. Within the membrane there are cylindrical proteins that allow certain chemicals to pass (gate for ions aka voltage gate chambers!!) if you just allow any ions to pass -> it can depolarize the membrane -> selectively permeable - allow some chemicals to pass more freely than others - e.g. O2, CO2, urea, water are uncharged and can pass - Ions: Na+, K+, Cl- can also pas
27
What is the sodium-potassium pump?
transports 3 Na+ out of cell and draw 2 K+ ins - sodium ions are 10x concentrated inside than outside
28
How does the sodium-potassium pump work to maintain electrical potential?
If channel open -> Na+ wants to enter Electrical gradient: Opposite charges attract (inside is more negative so more positive potassium ion wants to enter) Concentration gradient: difference in distribution of ions across membrane (Conc sodium inside < Conc sodium outside = wanna go in, however conc of potassium ion inside>outside, therefore wants to leave wants to even out by leaving)
29
Why must we maintain a resting potential?
Excitation of the neuron opens sodium channels, letting sodium enter the cell rapidly. Because the membrane did its work in advance by keeping so much sodium outside, the cell is prepared to respond vigorously to a stimulus. - like a bow arrow when pulled in advance vs at rest
30
What is action potential?
messages sent by axons
31
What is hyperpolarization?
increased polarization
32
What is depolarization?
reduce polarization toward zero
33
What does it mean the potential reaches threshold?
Membrane opens its sodium channels and permits sodium ions to flow into cell -> drive membrane potential upward (peak action potential: +30mV)
34
What is the all-or-none law?
the amplitude and velocity of an action potential are independent of the intensity of the stimulus initiated, provided that stimulus reaches threshold = pressing harder on light switch doesn't mean light is brighter - constrain how an axon send message - can change frequency of action potentials
35
What is the propagation of the action potential?
transmission of action potential down an axon -> aka new action potential "born" at each point along the axon - When action potential propagates, it also back-propagates into a dendrite - Cell body and dendrite DO NOT conduct action potential but registers the electrical event that started - Allow dendrite to be more susceptible to change
36
What are the two parts of the refractory period of action potential?
1. Absolute refractory period: time when membrane cannot produce an action potential, regardless of stimulation - FOR A MILISECOND after peak, sodium channels shut tight - so no movement - if membrane could produce another action potential -> would go to permanent depolarization 2. Relative refractory period: for 2-4 ms, sodium channel relax a bit --> (rapid departure of potassium ion - electrical potential more negative) -> need to have stronger than usual stimulus to initiate action potential
37
What is saltatory conduction?
Action potential jumps from node to node - helps to conserve energy as you need to only admit sodium ions at ever node of Ranvier - Myelinated axon: axon covered in myelin sheath - Nodes of Ranvier: axon not covered in myelin sheath
38
What occurs in multiple sclerosis?
In multiple sclerosis (hardening of fibers) -> immune system attack myelin sheath -> when axon lose myelin sheath, it also doesn't have the sodium chamber -> the action potential will die out btw one node to the next -> can cause visual impairment + muscle coordination problems
39
What is Charles Scott Sherringon (1906) known for?
Demonstrated neurons communicated at a junction, synapses - thru his studies of reflexes He strapped a dog and pinched its feet and saw it made a reflex (raised the leg but extent other leg) -> cut its spinal cord from brain, yet dog made same reflex His conclusion - Reflexes slower than conduction along axons - several weak stimuli presented at nearby places combine its effect - when one muscle set becomes excited, other muscle relaxes
40
What is Charles Scott Sherrington's evidence for synapse delay?
- when he pinch dog's foot, dog flexed after short delay -> what it showed-> impulse had to travel up an axon from skin receptor to spinal cord, then impulse travel down the leg to the muscle - Delay must be caused due to time taken for neurons to communicate to each other
41
What is temporal summation?
Repeated stimuli within a brief time combined its effect - light pinch did not evoke reflex but a few rapidly repeated pinches did
42
How does temporal summation work?
Single subthreshold excitation (EPSP) in post synaptic neuron decays over time -> with each rapid pinch -> effects adds from previous one -> combination of EPSPs exceeds the threshold of postsynaptic neuron -> produce action potential
43
What is Excitatory postsynaptic potential (EPSP)?
graded depolarization - sodium ions entering the neuron
44
What is Inhibitory postsynaptic potential (IPSP)?
graded hyperpolarization - produced by flow of negatively charged chloride ions into cells
45
What is spatial summation?
summation over space - he pinched super weakly BUT at two spaces at a time -> cause a reflex
46
How does spatial summation work?
Pinching two points activated sensory neurons whose axons converged onto a neuron in the spinal cord -> excitation from either axon excited that spinal neuron -> combination of excitation exceeds the threshold to produce an action potential
47
What is the spontaneous firing rate of a neuron?
Neuron have a spontaneous firing rate where periodic production of action potentials even without synaptic potential - EPSPs increases freqeuncy fo action potential above spontaneous rate - IPSP decreases it
48
What is Otto Loewi known for?
Proved synapse transmission is MOSTLY chemical and not electrical: essentially caused on frog heart to accelerate and used the fluid around the heart and put it on a second frog heart, and that heart rate also accelerated
49
How does synapse transmission works?
1.Neuron synthesis chemicals that serve as neurotransmitters, in the cell body or end of axon 2. Action potential travel down axon -> at presynaptic terminal, depolarization allows calcium to enter cell -> calcium release neurotransmitter from terminals into the synaptic cleft (space between presynaptic and postsynaptic neurons) 3. Released molecules bind to receptors and alter the activity of the postsynaptic neuron in any of several ways 4. Neurotransmitter molecule reuptake by transporter protein or diffuse away 5. Postsynaptic cell send reverse message to control the further release of neurotransmitter by presynaptic cells
50
What is the two most important types of neurotransmitters?
1. GABA, an amino acid, is the most important inhibitory neurotransmitter in the brain 2. Glutamate is the most important excitatory neurotransmitter in the brain
51
What is exocytosis?
when the calcium entry cause a burst of release of neurotransmitter from the presynaptic neuron (during synapse transmission)
52
Where are neurotransmitters stored?
vesicles - at the presynaptic terminal
53
How does neurotransmitter affects the postsynaptic receptor?
Ionotropic effect: when neurotransmitter binds to an ionotropic receptor Metabotropic effect: When neuromodulators bind with metabotropic recepto
54
How does the ionotropic effect occurs?
when neurotransmitter binds to an ionotropic receptor -> twist receptor just enough to open its central channel -> give a quick but short effect (5ms) - Channel controlled by neurotransmitter is called a Transmitter-gated or Ligand-gated
55
How does the metabotropic effect occurs?
When neuromodulators bind with metabotropic receptor -> bends the receptor protein that goes into the membrane of the cell -> other side of that receptor is attached to a G protein (protein coupled with guanosine triphosphate, energy storing molecule) -> detaches G protein -> lead to increase of second messenger inside the cell -> may open or close ion channels in membrane or activate or inactivate part of a chromosome -> give slow but long lasting effect (last a few seconds)
56
What is the difference between ionotropic effect and metabotropic effect?
Ionotropic effect: vision and hearing - immediate, brief information Metabotropic effect: taste, smell and pain - functions that arise slowly and last longer than a sensation - important for arousal, attention, hunger, thirst and emotions
57
What are the difference between neurotransmitter and neuropeptides?
Place synthesided: presynaptic terminal vs cell body Place released: Axon terminal vs mostly dendrites, also cell body and sides of axons Released by: Single action potential vs Repeated depolarization Spreed of effects: effect mostly on receptors of adj. postsynaptic cell vs diffuse to wide area Duration: milliseconds to seconds vs minutes
58
How do drugs chemically affect us?
1. Bind to neurotransmitter receptor - Drugs, esp hallucinogenic drugs, chemically resemble a neurotransmitter -> bind the receptor - E.g. LSD bind to serotonin receptors 2. Simulating release - MDMA (Ecstasy) releases dopamine/serotonin 3. Blocking reuptake - Amphetamine/Cocaine block reuptake of dopamine, serotonin and norepinephrine - Anti depressants also block reuptake but more weakly than cocaine - Prolong effect of neurotransmitter e.g. dopamine, serotonin and norepinephrine -> increase arousal BUT also enzyme break down extra dopamine that stays in synaptic cleft -> presynaptic cell need more time to replenish supply -> user has lass than usual dopamine -> withdrawal 4. Negative feedback - cannabinoids excite negative feedback receptors on the presynaptic neuron - Inhibit release of transmitter -> this is why is can help decrease anxiety
59
Are there electrical synpases?
There are electrical synapses BUT only for a few special synapses - Electrical transmission is faster than chemical - E.g. cells that control our breathing -> improtant we inhale on left side at the same time on the right
60
How do electrical synapses work?
- Membrane of one neuron makes direct contract of membrane of another - gap junction -> pores of membrane are lined up and always open -> allow sodium and other ions to pass -> when one of neuron is depolarized -> sodium ions from that cell pass immediately into other neuron and depolarize it too -> the two neurons act as if they were a single neuron
61
What is the central nervous system?
brain and spinal cord
62
What is the peripheral nervous system?
Connect brain and spinal cord to rest of the body
63
What are the two parts of the peripheral nervous system?
Somatic nervous system: axons that send messages from sense orgarns to the CNS and from CNS to muscles Automatic nervous system: controls body organs
64
What is the enteric nervous system?
Special part of the automatic nervous system that controls the digestive system
65
What does dorsal mean?
towards the back
66
What does ventral mean?
Toward the stomach
67
What is the coronal/frontal plane?
Plane that shows brain seen at the front
68
What is horizontal/tranverse plane?
A plane that shows brain structure as seen from above
69
What is the Sagittal plane?
A plane that shows brain structure as seen from the side
70
What is a lamina?
A row or layer of cell bodies separated from other cell bodies by a layer of axons and dendrites
71
What is a column?
a set of cells perpendicular to the surface of the cortex, with similar properities
72
What is a tract/projection?
a set of axons within the CNS - If axons extent from cell bodies in structure A to synapse B = fibers project from A onto B
73
What is a nerve?
A set of axons in the periphery, either form the CNS to a muscle or gland from a sensory organ to the CNS
74
What is a nucleus in terms of parts of the nervous system?
a cluster of neurons cell bodies within the CNS
75
What is the ganglion?
A cluster of neurons cell bodies, usually outside the CNS (as in sympathetic nervous system)
76
What is the gyrus?
A protuberance of the surface of the brain
77
What is the Sulcus?
A fold or groove that separates one gyrus form another
78
What is a fissure?
A long, deep sulcus
79
What is white matter?
Myelinated axons connecting neurons throughout the CNS
80
What is gray matter?
Cell bodies and dendrites
81
How does the spinal cord work?
Entering dorsal roots (axon bundles) carry sensory information and exiting ventral roots carry motor in formations - cell bodies of sensory neurons are in clusters outside spinal cord called dorsal root ganglia - cell bodies of motor neurons are inside spinal cord
82
What are the two parts of the autonomic nervous system?
Sympathetic nervous system: fight or flight parasympathetic nervous system: rest and digest
83
What is the hind brain?
The posterior part of the brain, that consist of the medulla, the pons and the cerebellum
84
What is the medulla/medulla oblongated?
Enlarged extension of the spinal cord - connected by 12 pairs of cranial nervous -Contributions to vital reflexes, damage is often fatal
85
What is the pons?
thickened part of the top of the medulla (ventral and anterior) - crossing over of many fibers in the motor and sensory pathways for contralateral motor control
86
What is the cerebellum?
small brain hanging under back of cortical hemisphere (dorsal and inferior) - automated movement, balance, timing and time perception, sensorimotor coupling, attention shifting Origin of cranial nerves: V - XII
87
What are parts of the midbrain?
Tectum: roof of the midbrain superior/inferior colliculi: contribute to sensory processing - Substantia nigra: contributes to movement initiation/rise to domapine containing pathways for readiness of movement - Origin of cranial verves: II - IV
88
What are the major components of the brain
Hindbrain: Contains the medulla oblongata, pons and cerebellum Midbrain: part of the brain stem, incl. sensory and motor relay nuclei Forebrain incl. hemisphere, corpus callosum and subcortical deep structures Brainstem: combination of structures of the forebrain, midbrain and hindbrain
89
What is the forebrain?
Contains Two cortical hemisphere - btw corext crumpled to increase surface area - further divided into 4 lobes Corpus callosum Structure under the cortex ("Sub cortex) which are: - thalamus - hypothalamus - pitugary glands - basal ganglia - hippocampus -The origin of the first cranial nerve (olfactory)
90
What is the thalamus?
Collection of smaller nuclei, sensory and motor parts -Relay station: sensory inputs travels through the thalamus to primary sensor areas, and motor output to the muscles -Gating mechanism: deciding what goes through, what gets attention
91
What is the hypothalamus
Just below the thalamus -Important for behaviour regulation - emotion and motivation - Food intake - activity level - sexual behaviour
92
What is the pituitary gland
- hormone-producing gland - responds to hypothalamus
93
What is the basal ganglia?
- Includes the putamen, caudate nucleus & globus pallidus -Exception in naming: ganglia are normally in PNS Primary motor functions - damaged in Parkinson's and Huntington's diseases - involved in movement initiation and vigour - also in motor sequence learning - also more abstract sequence learning - Timing
94
what is the hippo campus
- Crucial for memory - Shrinks in patients with Alzheimer's Disease - Named for seahorse (latin for seahorse)
95
What are ventricles and cerebrospinal fluid (CSF)?
-hollow spaces you see inside the brain are called ventricles, filled with fluid - CSF is produced by the gila cells that line the ventricles, and is circulated along the spinal cord - CSF cushions the brain when the head receives a shock of any kind
96
What does lateral mean?
towards the side, away from midline
97
What does medial mean?
toward the midline, away from the side
98
What is the term called if a structure is on the same side of the body?
Ipsilateral
99
What is the term called if the structure is one on the left and one on the right?
Contralateral
100
What are the 4 lobes in the cerebral cortex?
Occipital, parietal, temporal, frontal
101
What is the occipital lobe?
- Visual information - posterior end of the the cortex - Posterior pole of occipital lobe is the primary visual cortex or striate cortex
102
What happens if you damage the striate cortex/primary visual cortex?
Damage = cortical blindness so damage to right side of striate cortex = blindness in left visual field - person with cortical blindness has normal eyes and pupilary reflexes but no conscious visual perception and no visual imagery (no dream)
103
What is the parietal lobe?
- lies between the occipital lobe and central sulcus, a deep groove in the surface of the cortex - Area posterior to central sulcus is the postcentral gyrus or primary somatosensory cortex - receives sensations from touch, muscle and join receptors (body sensations)
104
What is the temporal lobe?
- Contains primary auditory areas - complex aspects of visual perception - memory (hippocampus)
105
What is the frontal lobe?
contains: precentral gyrus: primary motor cortex (posterior portion) - control of fine movements prefrontal cortex (anterior portion): contributes to many functions - working memory, planning, response initiation or inhabitation, impulse control
106
Damage to the Broca's area causes what?
Speech impairment/lost ability to speak
107
What is an ablation?
removal of a brain area with a surgical knife
108
What is a lesion?
Damage to organ
109
What is a stereotaxic instrument?
a device for the precise placement of electrodes in the brain
110
How does the eye work?
Light enters thru opeining in the centre of the iris, pupil -> focused by lens (adjustable) and cornea (not adjustable) -> projected on the retina -> retina lined with visual receptors -> light on left side strike right side of retina and vice versa, light on above strike bottom of retina and vice versa => image is reversed
111
What is the route within the retina?
When light hit retina -> message from receptors go back to eye to bipolar cells -> bipolar cells send message to ganglion cell -> ganglion cell's axons to form the optic nerve and exits thru the back of the eye -> the point where it leaves is a blind spot
112
What are amacrine cells?
Aid in refining response of bipolar and ganglion celll - enable to repsone to shaps, directions of movement, colour Cell that get information from bipolar cells and sends to other bipolar cells, ganglion cells and amarcrine cells
113
What is the fovea?
Central portion of the retina -> specialized for acute detailed vision
114
How is the fovea enable detailed vision?
Blood vessels and gangilion cell axons are almost absent near fovea -> unimpeded vision Tight packing of receptors (cones only) aid perception of details -> Each cone connects to single bipolar cell, that connects to single ganglion cell that has axon to brain (these ganglion cells are called midget ganglion cell - due to small and response to each cone)
115
How does periphery vision work?
Towards periphery of retina -> more and more receptors (rods + few cones) converge onto bipolar and ganglion cells -> summation enables perceptions of fainter lights in periphery -> HOWEVER, each bipolar and ganglion cell is excited by many rods -> loses information about the exact shape or location of an object
116
What is the differnce between human foveal and peripheral vision?
Receptors: cones only vs portion of rods increase toward periphery Convergence of input: each ganglion cell excited by one cone vs each ganglion cell excited by many receptors brightness sensitivity: distinguishes among bright light; respond poorly to dim lights vs response to dim light; poor for distinguishing among bright lights Sensitivity to detail: good detail vision as each cone's midget ganglion cell send msg to brain vs poor detail vision as many receptors converge to give input to given ganglion cell Color vision: good (many cones) vs poor (few cones)
117
What are rods?
Abundant in periphery of human retina -> respond to faint light - less useful in daylight -> bright light bleaches them - night vision
118
What are cones?
Abundant in and near fovea -> useful in bright lights and essential for color vision
119
What are photopigments?
Chemicals that release energy when struck by light, in both rods and cones. Photopigments consist of 11-cis-retinal (derivative of Vit. A) bond to proteins called opsins, that modify the photopigment's sensitivity to different wavelengths of light -> light converts 11-cist-retinal to all-trans-retinal, thus releasing energy that activates second messenger within the cell
120
What is the range of visible light?
Electromagnetic radiation within less than 400nm (violet) to more than 700nm (red)
121
What is trichromatic theory of color vision or Young-Helmoholtz theory?
We perceive color through the relative rates of response by three kinds of cones, each one maximally sensitive to a different set of wave lengths (short, medium and long)
122
What is opponent process theory?
We perceive color in terms of opposites - has a mechanism that perceives color on a continuum from red to green, another from yellow to blue, and another from white to black. After you stare at one color in one location long enough, you fatigue that response and tend to swing to the opposite.
123
How does opponent process theory work?
A bipolar cell receives excitation from medium wave length & inhibits from long wavelength cones -> increase activity to response to medium wave length light (green) and decrease response to red light -> after prolonged exposure to green light -> fatigued cell decreases cell -> because low level response by that cell = red, you see red
124
What is the main issue with the trichromatic theory and the opponent process theory?
Can't easily explain color constancy; ability to recognize colors despite changes in light
125
What is the retinex theory?
Cortex compares information from various parts of the retina to determine brightness and color for each area.
126
How does color deficiency comes about?
Color vision deficiency results when people with certain genes fail to develop one type of cone, or develop an abnormal type of cone
127
What is the organization of the retina?
Rods and cones make synapses with horizontal cell and bipolar cells -> horizontal cells make inhibitory contact onto bipolar -> bipolar cell makes synpases onto amacrine cells and ganglion cells -> axons of ganglion cell make optic nerve
128
How does the visual system connects to the brain?
Optic nerve travels along lower surface of brain until both optic nerve of both eyes meet at optic chiasm -> half of axons of each eye cross to opposite side of brain ie information from nasal half of each eye crosses to contralateral hemisphere -> most go to the lateral geniculate nucleus of the thalamus -> communicates with the visual cortex
129
What is lateral inhibition?
Helps sharpen contrast of a stimuli - eye nose, touch, sound
130
How does lateral inhibition work in the retina?
Light strikes the rods and cons -> decreases their spontaneous output -> receptors make inhibitory synapses onto the bipolar cells -> decreasing rods and cones inhibitory output -> decreased inhibition means net excitement
131
What is an receptive field?
area in visual space form which light excites of inhibits the cell
132
As we progress from bipolar cells to ganglion cells to later cells in the visual system, are receptive fields ordinary larger, smaller or same size?
Larger -> rods and cones are tiny receptive fields that connect to a bipolar cell with receptive field of all that combine > bipolar reports to ganglion and therefore have larger receptive field
133
What are the 3 kinds of primate retina ganglion cells?
Parvocellular neurons, magnocellular neurons, and koniocellular neurons
134
What are parvocellular neurons?
Most numerous, help respond to detailed shapes, small cell bodies, with small receptive fields and chill in the near fovea + colour sensitive
135
What are magnocellular neurons?
help with movement and broad outlines of shape, large cell bodies and large receptive field, throughout the retina but not color sensitive
136
What are koniocellular neurons?
Variety of functions, some are color sensitive, throughout the retina and mostly small but variable and have small cell bodies
137
What happens if you damage area V1/primary visual cortex/striate cortex?
No conscious vision, no visual imagery and no visual dreams - may display phenomenon called blind sight: ability to respond to visual information without perceiving it consciously
138
What are the cells in the primary visual cortex?
Simple cell, complex cells and end-stopped or hypercomplex cell
139
What is an simple cell?
Located in V1, respond to stimulus in only one location - has receptive field (smallest) - bar or edge shaped with fixed excitatory and inhibitory zones
140
What are complex cells?
Located in V1 and V2 - medium receptive field - respond to a stimulus anywhere - bar or edge shape
141
What are end-stopped cells?
located v1 and v2, - same as complex cell but has strong inhibitory area
142
What are feature detectors?
neurons whose response indicate the presence of a particular feature
143
What is strabismus?
Lazy eye
144
How is information passed in the visual cortex?
Primary visual cortex (V1) sends information to secondary visual cortex (V2) which process information further and transmit it to other additional areas (V3, V4 and V5) - V2 and V3: highly responsive to color and disparity btw. left and right eye - V4: cluster of cells responsive to specific colors - inferior temporal cortex
145
What is the difference between the ventral and dorsal streams of the visual system?
Ventral stream thru the temporal cortex is the "what" pathway - importance for identifying and recognizing objects Dorsal stream thru the parietal cortex is the "where" and "how" pathways - importance for visually guided movements
146
What happens if you have damage in your ventral steam/temporal cortex?
- cannot recognise objects but can guide actions
147
What happens if you have damage to your dorsal stream/parietal cortex?
Can recognize things, can read ect but cannot perceive shit around them, would bump into things
148
What is the inferior temporal cortex?
Learn to recognize familiar objects - inferior cortex exchange information with prefrontal cortex with connections that are important for identifying difficult or ambiguous patterns
149
What happens if you damage the ventral pathway of the inferior temporal cortex?
Visual angosia: inability to recognise objects despite otherwise satisfactory vision - e.g. one dude can see everything but numbers 2 - 9
150
Damage to the fusiform gyrus does what?
Unable to recognise faces (prosopagnosia)
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What is the middle temporal cortex (v5) and areas MST (medial superior temporal cortex)?
receives input from mostly magnocellular paths - detects overall patterns and movement - color insensitive
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What happens if you damage area MT (V5) and MST?
Motion blindness: able to see objects but unable to see whether they are moving
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How do we hear?
Sound wave passes through the auditory canal -> enter middle ear -> they vibrate the ear drum/tympanic membrane -> tympanic membrane connects to 3 tiny bones (hammer, anvil and stirrup) that transmit the vibration to the oval window -> vibrations from ear drum is amplified to forceful vibrations of smaller stirrup -> convert sound waves into greater pressure on oval window -> sets the motion the fluid in cochlea (snail thingy) -> hair cells lie along basilar membrane of cochlea -> vibration in fluid of cochlea displace hair cell -> stimulate auditory nerve
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What is place theory?
Basilar membrane varies from stiff at its base, where stirrup meets cochlea, to floppy at other end of cochlea, the apex. High pitch sound travels and peaks sharply at some point along basilar membrane. Low frequency sound vibrate hair cells near apex and high frequency sounds, vibrate hair cells farther toward base
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What happens when you damage the primary auditory cortex (Area A1)?
Not deafness but people have trouble with speech and music -> can identify single sounds but cannot really process what information means + important for thinking about anything you heard - can't tell a word is real because you are unable to imagine how the word sounds like
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What is amusia?
Tone deafness -> unable to detect a change less than about the difference between C and C sharp - cannot tell whether some one is singing off key - Auditory cortex has less connections to frontal cortex than average
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What is conductive/middle-ear deafness?
when bones in middle ear unable to transmit sound waves properly to the cochlea - cant be corrected with surgery - have normal cochlea and auditory nerve
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What is nerve/inner ear deafness?
Damage to cochlea, the hair cells or auditory nerve - if confide to one part of cochlea, it impairs hearing of certain frequencies - can be inherited
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What is tinnitus?
frequent or constant ringing in ear - damage like phantom pain - if auditory cortex no longer gets normal input, other axons invade the deprived area
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What is the vestibular system?
Help guiding eye moment and maintaining balance
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Where is the vestibular organ located?
Wrapped around the cochlea
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What does the vestibular organ consist of?
3 semicircular canals, orientated in perpendicular planes, filled with fluid and lined with hair cells -> acceleration of head -> cause fluid to splash -> push against hair cells -> set up action potential
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How does somatosensation work in the CNS?
Each spinal nerve have sensory competent and motor competent - each connected to limited area of body called a dermatome - travel thru spinal cord towards thalamus -> send impluse to different areas of the primary somatosensory cortex in parietal lobe
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What happens if the primary somatosensory cortex s1, is damaged?
Impair body perceptions - phenomena known as numbsense -> have to guess location of touch while not being able to feel it
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How do we taste?
Rceptors are taste buds on the papilla of the tongue - Intended to signal healthy foods - Traditional tastes: sweet, sour, salty, bitter, ‘newer’ tastes: umami and oleogustus - Large individual differences in sensitivity, partly accounted for by genetic factors and hormones
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How do we smell?
- Receptors are inside the nose, based on airborne substances - Sense of flavor in taste mostly dependent on smell - Sensitivity influenced by hormones
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What is the development of neurons?
Proliferation - birth of new primitive cells in the ventricles Migration: primitive cells migrate to their destination (Radial gila) Differentiation: primitive cells become neurons or gila cells Synaptogenesis: formation of synapses Myelination: gila start producing insulating fatty sheaths (from caudal to rostral)
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How did Roger Sperry showed pathfinding by axons?
Cut optic nerve in newt -> rotated eye by 180degrees -> axon that is for dorsal portion on retina, now ventral grew back to area for vision to dorsal retina aka other parts grew back to original target -> newt saw world upside down and reversed
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What is apoptosis?
Programmed mechanism for cell death
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What substances can prevent apoptosis?
Neurotrophines (Chemical that promotes survival and activity of neurons) e.g. NGF - nerve growth factor - a protein that promotes the survival and growth of an axon when a neuron form a synpase onto a muscle BDNF - Brain-derived neurotrophic factor
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Why do neurons have a spontaneous firing rate?
One reason: neurons are active get more of these neurotrophins -> keeping as many neurons alive -> allows for plasticity - Neurons that fire together, wire together - Donald Hebb
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What is focal hand dystonia?
neurological disorder that causes involuntary muscle contractions in the hand.
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How does a musician develop focal hand dystonia?
When brain reorganized too much -> play instrument a lot -> representation of hand increase in somatosensory cortex -> representation of all fingers grow from side to side without spreading out -> each finger overlaps with neighbor -> can't feel difference between one finger and another - two fingers start to feel and move as one
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What is cerebrovascular accident?
type of brain damage- temporary interruption of normal blood flow to a brain area during a stroke
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What are the two types of strokes?
Ischemia (More common): result of blood clot or other obstruction in an artery Hemorrhage (not common): result of ruptured artery
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What happens when you get ischemia (stroke)?
Neurons deprived of blood lose much of their oxygen and glucose supplies + Cerebrospinal fluid (CSF) flows into brain and rapidly accumulates -> cause swelling -> impair sodium-potassium pump -> excess sodium release excess glutamate-> overstimulates neurons -> cause damage
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What happens when you get an hemorrhage (Stroke)?
neurons are flooded with blood and excess oxygen, calcium and other chemicals -> cause edema (accumulation of fluid) -> impair sodium-potassium pump -> excess sodium release excess glutamate-> overstimulates neurons -> cause damage
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How do you treat a stroke?
1. Breaking up Blood Clots - tpA: tissue plasminogen activator Reduce over stimulation - blocking glutamate receptors, cannabinoids decrease glutamate release Other: cooling the brain, antioxidants, antibiotics (to counteract infection), albumin (against brain swelling), treatments targeting the immune system
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What is diaschisis?
Decreased activity of surviving neurons because of damage to other neurons/reduced activity in connected neurons
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What is denervation super sensitivity?
Increased sensitivity in remaining synapses (after brain damage) - to compensate for decreased input
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What is collateral sprouting?
when cell loses input from axon -> creates neurotrophines that induce other axons to form new branches that take over vacant synapses
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How does phantom limb pain come about?
Relevant portion of the somatosenory cortex reorganizes and becomes responsive to alternative inputs -> e.g. axons representing face come to active the cortical area which was previously for amputated hand -> touch to face now produce farcical sensation + phantom hand sensation yes so since cortex responsive to feet adjacent to genitals -> two patients with amputations felt phantom foot during sexual arousal
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What is memory?
One of the higher cognitive functions, related to: 1. the processing and storing of information (sensory impression, learning, experiences) - learning new things 2. retaining information for shorter or longer periods of time 3. recognizing or actively recalling information (bring previously processed and stored information back to consciousness)
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What are the difference between long term and short term memory?
Capacity: unlimited vs 4-7 items type of learning: 1 shot learning - rehearsal required Retrieval: hints help vs lost = lost duration: 30s to decades vs seconds to minutes
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What are the 2 types of long term memory?
Episodic memory: personal events Semantic Memory: factual knowledge
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What are the two types of short term memory?
Sensory memory: Sensory buffer: containing recent sensory experiences * Large capacity; short-lived * Visual trace * Auditory trace working memory: way we store information while working on it - limited capacity of 4ish items - delayed response task
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What makes someone more prone to Alzheimer's Disease?
APOPE gene - protein that contributed to many functions - if you have 1 copy of type 4 gene, APOPE4, you are 4 xthe normal risk of Alzheimer's and if you have 2 copies, you are 15x more risk B-amyloid and tau protein accumulation in neurons -> both spread within cells and from cell to cell disrupt neurotransmitter, damaging mitochondria and triggering waves of microgram to kill neurons - damaged dendrites and axons cluster tgt in plaques -> cascade hypothesis: large amount of amyloid-B cause changes in tau proteins, ultimately leading to tau buildup and tangles
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What is infant amnesia?
not a disorder - unable to remember what happened in first few years of life
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What is procedural memory?
How to do things/procedures e.g. how to ride bike
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What is retrograde amnesia?
loss of memory of events that took place before brain damage (long term memory)
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What is anterograde memory?
inability to form new memories after brain damage (short term memory)
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What is Wernicke-Korsakoff syndrome?
Caused by thiamine deficiency (Vit B1) - extreme alcoholism/anorexia Unique symptom: Confabulation (fabricated/distorted memories) * Similar to prefrontal disorder: apathy, confusion and memory loss
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What type of memories that patients with Korsakoff's syndrome have intact and imparied?
Impaired: WM/STM & LTM: episodic memory + confabulation Intact: LTM: semantic memory, procedural memory
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What is alzheimer's disease?
Common in old - Gradual increase in memory loss, confusion, depression, restlessness, insomnia, and reduced appetite - patients with down syndrome often develop AD by middle age
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What are the types of memory that patients with Alzheimer's disease?
Impair: STM/WM & LTM: Episodic memory Intact: LTM: Semantic memory, procedural memory, other symptoms: reduced alertness
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Why do we have childhood amnesia or why we forget them?
Hypotheses: o Learning language and complex reasoning abilities don’t develop until the child is older o Changes in the hippocampus and growth of new neurons
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What is the case of HM (Henry Maison)?
Severe epilepsy - removed hippocampus + bilateral medial temporal lobe - treated seizures but severe memory impairment Medial temporal lobe removal led to impairment: - LTM: Episodic memory - LTM: Storage - anterograde, retrograde, emantic Intact: procedural memory +STM/STM, had better implicit memory than explicit memory
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What is implicit and explicit memory?
Implicit memory: influence of experience on behavior - like comfortable with psychologist but he dosent remb their name or where he met them Explicit/declarative memory: deliberate recall of information that one recognize as memory
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What does damage to the hippocampus causes?
Impairs 1. Delayed matching-to-sample task - Subject sees an object and must later choose the object that matches 2. Delayed nonmatching-to-sample tasks - Subject sees an object and must later choose the object that is different from the sample
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What is the functions of hippocampus?
* Recent memories with a lot of contextual detail are hippocampus-dependent * Older memories with less contextual details are more dependent on the cerebral cortex * Navigation and spatial orientation
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What evidence do we have that shows hippocampus role in navigation and spatial orientation?
Radial maze - rats have to explore multiple arms to find food, rat with damaged hippocampus can learn to avoid never correct arms Morris water maze - rat swim thru murkey water to find rest platform that is under surface -> if rest platform stays same location, rat with hippocampal damage can learn to find it
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How does spatial memory work?
Hippocampus * Place cells: That respond to a certain location or when a route is planned - cells reorder themselves to map out new locations * Time cells: Coding for orientation in time - cell activate at certain time during the 20s a rat had to run Entorhinal cortex * Grid cells: Coding for a location in a hexagonal grid
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What does the basal ganglia consist of?
Globus pallidus + subthalamic nucleus + substantia nigra + striatum Striatum = caudate nucleus + putamen
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What type of learning is the striatum responsible for?
Habits, implicit + specialised in probabilistic learning - you know it but can't explain it - depends on basal ganglia
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What type of learning is the hippocampus responsible for?
Declarative/explicit
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What are the differences btw the hippocampus and striatum?
Speed of learning: can learn in single trial vs learns gradually over many trials Type of behavior: flexible responsible vs habits Based on what type of feedback: sometimes connects information over a delay vs generally requires prompt feedback Explicit or implicit learning: explicit vs implicit What happens after damage: impaired declarative memory, esp. episodic memory vs impaired learning of skills and habits
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What is the Hebbian synapse?
- A synapse that increases in effectiveness because of simultaneous activity in the presynaptic and postsynaptic neurons (neurons that fire together, wire together) - Such synapses may be critical for many kinds of associative learning
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What is habituation?
Decrease in response to a stimulus that is presented repeatedly and accompanied by no change in other stimuli
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What is sensitization?
Increase in response to mild stimulus as a result to previous exposure to more intense stimuli
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What is long-term potentiation (LTP)?
when one or more axons bombard a dendrite with stimulation, and leaves the synapse “potentiated” (more responsive to new input) for a period of time making the neuron more responsive - synaptic connection btw neurons become stronger with frequent activation - underlying basis for learning and memory
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What are the three properties that affect Long Term Potentiation?
*Specificity: only synapses onto a cell that have been highly active become strengthened * Cooperativity: simultaneous stimulation via two or more axons produces LTP much more strongly than does repeated stimulation by a single axon *Associativity: pairing a weak input with a strong input enhances later responses to a weak input
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What is Long-term Depression (LTD)?
a prolonged decrease in response at a synapse, occurs for axons that have been less active than others
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Where does LTP occurs most?
Hippocampus - sometimes at GABA synpases but mostly at glutamate synapses
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What is the biochemical mechanism behind Long Term Potentiation?
When glutamate massively stimulated AMPA receptors -> resulting depolarization enables glutamate to stimulate nearby NMDA receptors -> stimulation of NMDA receptors let calcium enter cell where it sets into motion series of changes that regulate gene expression to build new glutamate synapses or increase responses to glutamate at existing AMPA receptors -> after LTP -> NMDA receptors revert to their previous condition
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How does the brain affect intelligence in humans?
Humans do not have the largest brain mass or brain-to-body ratio, but we do have the largest number of brain neurons - Newer research with more accurate measurements has revealed a moderate correlation (.24): With larger brain size associated with a higher IQ - IQ mainly correlates with grey matter surface in especially frontal and parietal regions
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What is the microcephalin gene?
A gene identified that influence the size of the neocortex * A causal link between the micropcephalin gene and microcephaly ( baby's head is significantly smaller than expected for their age and sex) * Zika disrupts the microcephalin gene (among others) * Down-regulates proliferation, migration and differentiation of neurons
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What is the proprioceptive system?
body awareness; location of your body in space
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What are reflexes?
- fixed, rapid, automatic movements triggered in response to a specific sensory stimulus - little voluntary control, but can be modulate e.g. eye blink
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What are postural movement?
-automated movement; combination of reflex and volition used to maintain an upright position with respect to gravity - e.g. vestibulospinal reflexes - stabalizing body position when head position moves
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What are rhythmic movement?
Automated movement; initiation and termination is voluntary, but actual movement is more stereotyped - e.g. walking, running, chewing
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What are voluntary movements?
- purposeful, goal-directed movements - initiated entirely from within the CNS - performance improves with practice - reflex and postural movements compensate for the effects of the intended action
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What are the 3 types of muscles vertebrates have?
Smooth muscles - control digestive system + organs Skeletal or striated muscles - control movement of body in relation to environment Cardiac muscle - control the heart
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How are muscles composed?
Composed of many fibers but each muscle fiber only receives information from one axon; but a single axon may innervate many muscle fibers
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What is a neuromuscular junction?
Synapse btw motor neuron axon and muscle fiber
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How does muscle function/how we move?
Movement requires the alternating contraction of opposing sets of muscles called antagonistic muscles e.g. to flex your bicep - bicep muscle contract while triceps muscle relaxes
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What is a flexor muscle?
One that flexes or raises a joint
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What is a extensor muscle?
One that extends or straightens a joint
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What is the biochemical mechanism for your muscle to contract or to relax?
An axon at a skeletal muscle releases acetylcholine at the neuromuscular junction, causing a muscle contraction. - MUSCLES CAN ONLY CONTRACT NO MESSAGE FOR relaxation or to move muscle in opposite direction NOTE: A deficit of acetylcholine or its receptors impairs movement.
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What are the two types of skeletal/striated muscles?
I) Slow-twitch: fibers produce less vigorous contraction without fatigue II) Fast-twitch: fibers produce fast contractions but fatigue rapidly NOTE: people have mix of both!
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What are the differences between slow-twitch muscles and fast-twitch muscles?
*Slow-twitch fibers are aerobic and require oxygen during movement and therefore do not fatigue - Nonstrenuous activities utilize slow twitch and intermediate fibers - fibers are red and dark - more o2 * Fast-twitch fibers are anaerobic and use reactions that do not require oxygen, resulting in fatigue - Behaviors requiring quick movements utilize fast-twitch fibers - fibers are light pink - less o2
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What are proprioceptors?
receptors that detect the position or movement of a part of the body
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What are the two kinds of proprioceptor receptors?
Muscle spindles & Golgi tendon organs
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What is a muscle spindle?
Proprioceptors parallel to the muscle that respond to a stretch: cause a contraction of the muscle -When the muscle is stretched, the muscle spindle sends a message to a motor neuron in the spinal cord, which in turn sends a message back to the muscle, causing a contraction - reflex provides negative feedback
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What is a stretch reflex
occurs when muscle proprioceptors detect the stretch and tension of a muscle and send messages to the spinal cord to contract it -caused by a stretch; it does not produce one.
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What is a golgi tendon organ?
*Type of proprioceptor that responds to increases in muscle tension - Located in the tendons at the opposite ends of the muscle - Acts as a “brake” against excessively vigorous contraction by sending an impulse to the spinal cord to inhibit motor neurons
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Is movement solely either voluntary or involuntary?
No! Most movements are a combination of voluntary and involuntary; reflexive and non-reflexive - Automatic production of walking pattern - Ability to voluntary change or stop Movements vary with respect to feedback- Some are ballistic and cannot be changed once initiated e.g. throwing ball super hard - Others are guided by feedback (perception + cognition!)
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What are central pattern generators?
neural mechanisms in the spinal cord that generate rhythmic patterns of motor output e.g. wings flapping in birds
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What is a motor program?
*Fixed sequence of movements that is either learned or built into the nervous system - Once begun, the sequence is fixed from beginning to end - Automatic in the sense that thinking or talking about it interferes with the action - Examples: mouse grooming itself; humans yawning
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What is the cerebral cortex role in movement?
The primary motor cortex (M1) is located in the precentral gyrus in the frontal lobe *Axons from the precentral gyrus connect to the brainstem and the spinal cord, which generate impulses that control the muscles - So, muscle control via M1 - Cerebral cortex is additionally involved in complex movements
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How do we plan a movement?
The primary motor cortex is active when people intend a movement -The primary motor cortex “orders” an outcome - Specific areas of the primary motor cortex (M1) are responsible for control of specific areas of the opposite side of the body - Some overlap does exist
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How does the posterior parietal cortex contribute movement?
keeps track of the position of the body relative to the world - Damage to this area causes difficulty in coordinating visual stimuli with movement - Important for planning movement Note: Posterior to the primary somatosensory cortex S1
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How does the premotor cortex contribute to the planning of movement?
- Active during preparation for movement- - Receives information about a target - Integrates information about position and posture of the body; organizes the direction of the movement in space NOTE: sandwiched btw the prefrontal cortex and primary motor cortex, anterior of the primary motor cortex
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How does the supplementary motor cortex contribute to movement
- Organizes rapid sequence of movements in a specific order; inhibitory if necessary - Active seconds before the movement - Active following an error in movement so you can inhibit the incorrect movement the next time -Damage to the area, people at first have only few and slight voluntary movements, but they report that they did not lack the desire to move. They simply could not get a movement started. NOTE: dorsomedial part of the frontal cortex
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How does the prefrontal cortex contribute to movement planning?
- Active during a delay before movement - Stores sensory information relative to a movement - Necessary for you to consider the probable outcomes of a movement - Damage: movement will be disorganized e.g. showering with clothes on, doing things absentmindedly = prefrontal cortex not fully awake aka me pouring the water in coffee when it aint boiled yet
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What is the difference between the premotor cortex vs the prefrontal cortex
* M1 and the PMC have direct connections to the spinal cord to control/produce movement * PFC areas influence M1 and the PMC, not the spinal cord
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What is the antisaccade task?
A saccade (sa-KAHD) is a voluntary eye movement from one target to another. Suppose a person is staring straight ahead when something to one side or the other moves. They have a strong tendency to look toward the moving object. In the antisaccade task, you are supposed to look as quickly as possible in the opposite direction.
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How does antisaccade task measure activity of prefrontal cortex?
Performing this task well requires sustained activity in parts of the prefrontal cortex and basal ganglia before seeing the moving stimulus - Ability to perform this task matures through adolescence (5-7 years old find it impossible to look away)
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What are mirror neurons?
*Active during both preparation of a movement and while watching someone else perform the same or similar movement (active in PMC) - May be important for understanding, identifying, and imitating other people - May be involved in social behaviors (autism?) - Unknown whether they cause or result from social
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How does the brain connect to the spinal cord for movement?
Messages from the brain must reach the medulla and spinal cord to control the muscles - Corticospinal tracts are paths from the cerebral cortex to the spinal cord Two such tracts: - Lateral corticospinal tract - Medial corticospinal tract
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What is the lateral corticospinal tract?
A set of axons from the primary motor cortex, surrounding areas, and red nucleus to the spinal cord - Controls movement in peripheral areas (hands and feet) - Red nucleus: a midbrain area with output mainly to the arm muscles - Axons extend from one side of the brain to the opposite side of the spinal cord, and control opposite side of the body
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What is the medial corticospinal tract?
* A set of axons from many parts of the cerebral cortex - Reticular formation, midbrain tectum, and vestibular nucleus - Vestibular nucleus is a brain area that receives information from the vestibular system - The medial tract controls the muscles of the neck, shoulders, and trunk - Responsible for bilateral movements like walking, turning, bending, standing up, and sitting down
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What is a cerebellum?
A structure in the brain often associated with balance and coordination - More neurons in the cerebellum than in all other brain areas combined - Damage to the cerebellum causes trouble with rapid movements requiring aim/timing- Examples: clapping hands, speaking, writing, and so on. - Important for the establishment of new motor programs that allow the execution of a sequence of actions as a whole; for example, tasks that require timing - responds to sensory information even in no movement + respond strongly to violations of sensory information
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How does processing in the cerebellum work?
-Recieves input from the spinal cord, from each of the sensory systems, and the cerebral cortex - Sends it to the cerebellar cortex -> cerebellar nuclei send output back to cerebral cortex
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What is the cellular organization of the cerebellum?
Surface of the cerebellum - Molecular cell layer - Purkinje cell layer - Granule cell layer Cerebellar cortex neurons are arranged in precise geometrical patterns that provide outputs of well-controlled duration Purkinje cells: flat parallel cells in sequential planes- Parallel fibers: axons parallel to one another; perpendicular to planes of Purkinje cells Parallel fibers excite Purkinje cells -> Purkinje cell transmit inhibitory messages to the cells in the nuclei of the cerebellum (clusters of cell bodies in the interior of the cerebellum) and the vestibular nuclei in the brain stem -> Messages are then sent to the midbrain and the thalamus ->The greater the number of excited Purkinje cells, the greater their collective duration of response
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How does the basal ganglia work?
Every area of the cortex interacts with the basal ganglia via recursive loop circuits - Two main pathways modulate cortical activity - Indirect pathway is inhibitory - Direct pathway is excitatory Caudate nucleus and putamen receive input from the cerebral cortex and send output to the globus pallidus -> Globus pallidus connects to the thalamus, which relays information to the motor areas and the prefrontal cortex- Inhibits the thalamus -> Basal ganglia select a movement to make by ceasing to inhibit it
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What is parkinson's disease?
- Characterized by muscle tremors, rigidity, slow movements, masked face, posture/gait issues - Associated with difficulty in initiating spontaneous movement in the absence of stimuli to guide the action
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How does parkinson's disease occur?
Associated with gradual and progressive death of neurons, especially in the substantia nigra - Substantia nigra usually sends dopamine-releasing axons to the caudate nucleus and putamen - Loss of dopamine leads to less stimulation of the motor cortex and slower onset of movements
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How does the brain connections (Basal ganglia) from a person with Parkison's disease look like?
Indirect pathway (inhibitory) becomes more active, leading to decreased excitation from the thalamus to the cortex Specifically -> decreased excitation from substantia nigra to putamen -> decreased inhibition from putamen to globus pallidus -> increase inhibition from globus pallidus to thalamus -> decreased excitation from thalamus to cortex
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What are the risk factors to Parkinson's disease (damaged substantia nigra)?
- Studies suggest early-onset Parkinson’s has a genetic link - Genetic factors are only a small factor of late onset Parkinson’s disease (after 50) - Environmental influences such as exposure to toxins - Insecticides, herbicides, and fungicides - Traumatic head injury - Lifestyle factors- Cigarette smoking and coffee drinking are related to a decreased chance of developing Parkinson’s disease - Damaged mitochondria of cells seems to be common to most factors that increase the risk of Parkinson’s disease
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What are the possible treatment to Parkinson's disease
Levodopa (L-dopa) - Primary treatment for Parkinson’s, golden standard - Precursor to dopamine that easily crosses the blood-brain barrier - Often ineffective and especially for those in the late stages of the disease - Does not prevent the continued loss of neurons - Enters other brain cells, chance of side effects ie nausea, restlessness, sleep problems Other possible treatments for Parkinson’s disease: - Drugs that directly stimulate dopamine receptors - Implanting electrodes to stimulate areas deep in the brain Experimental strategies such as: - Transplanting brain tissue of aborted fetuses - Implantation of stem cells that are programmed to produce large quantities of L-dopa
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What is Huntington's disease?
A neurodegenerative disease caused by a dominant genetic mutation - Affects 1 in 10,000 in the United States; onset between age 30-50 - The gene produces huntingtin, and the altered form is toxic to the caudate and putamen - Associated with gradual and extensive brain damage especially in the basal ganglia but also in the cerebral cortex
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What are the symptoms of Huntington's disease
*Patients display non-voluntary rhythmic movements (chorea) - Overstimulation of the motor drive (opposite to Parkinson's Disease) Initial motor symptoms include arm jerks and facial twitches -Motor symptoms progress to tremors and writhing that affect the persons walking, speech, and other voluntary movements -Also associated with various psychological disorders: - Depression, memory impairment, anxiety, hallucinations/delusions, poor judgment, alcoholism, drug abuse, sexual disorders
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How does heredity and presymptomatic testing play a part in Huntington's disease
* Presymptomatic tests can identify with high accuracy who will develop the disease - Controlled by an autosomal (not on X or Y chromosome) dominant gene on chromosome #4 (yes, single mutant gene) - The higher the number of consecutive repeats of the combination C-A-G (cytosine, adenine, guanine), the more certain and earlier the person is to develop the disease
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What are emotions?
are short-lived, affective responses to internal or external stimuli in the service of adaptive behaviour Cognition - Affect - Physiological response - Action
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What is James-Lang theory of emotion?
Stimulus -> autonomic arousal -> conscious feeling ie you feel afraid because you run awa Action (physiological action/response) before Emotion
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What evidence supports James-Lange Theory of emtion?
Facial-feedback hypothesis: smiling make you feel happier ect - people with botox said they felt less intense emotions than people without botox felt when showed the same stimulus
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What are the criticism to the James-Lange Theory?
1. Physiological events do not guarantee emotion 2. Physiological events may not precede emotion 3. Identical physiological events are associated with several different emotions
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What is the Canon-Bard theory of emotion?
Stimulus -> subcortical brain activity -> leads to both conscious feeling + autonomic arousal (physiological response & emotion)
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Do people have limited number of basic emotions?
Original thought of 6 emotions: Happiness, Anger, Sadness, Surprise, Disgust, Fear - Original study sucked: Use MCQ to choose lmao Emotions require context!!!
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What is the theory of constructed emotions (Lisa Feldman Barrett)?
Emotions are brain predictions that connect bodily states to events in the environment so that the person knows how to (re)act -Emotion is a socially constructed category that people find useful
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Are there specific brain regions that activate when we feel a type of emotion?
Nope, PET and fMRI scans show there is high variability of locations for each emotion
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What is the behavioral activation system (Approach)?
Left brain hemispheric activity marked by low to moderate autonomic arousal and a tendency to approach, which could be either happiness or anger
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What is the behavioral inhibition system (Avoid)?
Right brain hemisphere activity, which increases attention and arousal, inhibits action, and stimulates emotions such as fear and disgust
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People with great activity in the frontal cortex left hemisphere tends to be
Happier, more outgoing, more fun loving
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People with great activity in right hemisphere tend to be
More socially withdrawn, less satisfied with life and prone to unpleasant emotions
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What are the functions of emotions?
1. Adaptive value (Fear, anger, disgust ect) 2. Help communicate needs to others 3. Help understand other people's needs and probable actions 4. Provide useful guide when we need to make a quick ("gut") decision 5. Moral decision: pay attention to how the outcome will make us feel
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What happens if you have prefrontal cortex damage?
Emotions are blunted + tend to make impulsive decision-making without pausing to consider consequences Case 1: Phineas Gage - impulsive and made poor decisions Case 2: Antonio Damasia - expressed no emotions -made bad decisions that cost his job, marriage and savings
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Are people equally good at recognizing facial expression?
No there is individual differences -> People with better connections between the frontal cortex and the anterior temporal cortex tend to be better at recognizing facial expressions.
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What is pure autonomic failure?
People whose autonomic nervous system completely or almost completely cease activity - organs continue to function BUT no nervous system to regulate them - continue to report emotional experiences, but the feeling aspect is weaker than before
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What do proness to approach, avoid and be anxious depends on?
1. The individual - genetic 2. Situation Attack and Escape behaviors are closely related physiologically and behaviourally
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What can a deficiency of monoamine oxidase A (MAOA) cause?
monoamine helps break down neurotransmitters like serotonin, dopamine and norepinephrine in reuptake to prevent excess accumulation deficiency MAOA -> increase in build up in serotonin in neuron -> increase risk of antisocial behaviour esp in all males -> MAOA gene is X linked - expected is less aggressive Lower activity of MAOA + SHITTY environment = more aggressive
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What hormones contribute to attack behaviors?
Testosterone: facilitates aggressive, assertive, and dominant behaviours Serotonin: tend to inhibit impulsive behaviours - lower level = higher impulsive anger Cortisol: Inhibits aggression
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What is serotonin turnover?
the amount that neurons released and replaced. -When neurons release serotonin, they reabsorb most of it and synthesize enough to replace the amount that washed away. - measured by concentration of 5 hydroxyindoleacetic acid (5-HIAA) in CSF
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Is aggression dependent on one chemical?
Does not strongly correlate strongly with one chemical - DEPENDS ON COMBINATION aggression depends on ratio testosterone: cortisol - dual-hormone hypothesis: aggression related to facilitation by testosterone and inhibition by hormone cortisol
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What is the startle reflex and why is it important in the study of emotions?
Response that one makes after a sudden, unexpected loud noise or similar sudden stimulus - it is universal across species
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How does damage to the amygdala affect the startle reflex?
Normal startle reflex, but signals of danger/safety do not modify the reflex -Amygdala is important for enhancing the startle reflex
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What does amygdala research tell us about the concept of fear?
Fear of pain, predators and aggressive members of the same species And fear is not a single indivisible state!!
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What is Klüver-Bucy syndrome?
Damage in amygdala in MONKEY - tame and placid - less than normal fear of snakes and larger, more dominant monkey - have impaired social behaviors, including learning what to fear
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What happens to people with damaged amydala?
Ability to classify emotions (cognition) however feel little arousal from viewing unpleasant photos (feelings) Have trouble identifying facial expression of fear
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What is Urbach-Wiethe disease?
genetic disorder that causes gradual atrophy of the amygdala Case of SM: - Experiences fearlessness - correctly drew faces with various emotions but had trouble drawing a fearful face - very close comfortable distance btw. her and another person - lack of fear is dangerous to her
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What evidence shows amygdala is important to fear reactivity?
College students with higher amygdala activity to frightening pictures (fMRI) - higher number of unpleasant emotions recorded in year before Soldiers with higher amygdala activity response experience more combat stress
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What is Bed nucleus of the stria terminalis?
A set of neurons that connect to the amydala
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What is Post Dramatic stress disorder?
Psychiatric disorder that occurs in some people had a trauma experience of being severely injured or threatened or seeing other people harmed or killed - exposed and ptsd person tend to have smaller hippocampus - smaller hippocampus may predispose you to PTSD
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What is a panic disorder?
condition marked by freq. periods of anxiety and rapid breathing, increased HR, sweating and trembling - women > men; transgender also high - adolescent and young adult > older adult
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What can relief us from anxiety?
Benzodiazepines: Anti-anxiety drugs - Bind to GABA receptor, a Cl- channel→ Change in receptor shape → GABA attaches more easily → GABA binds more tightly -> GABA twists receptor to open chloride channel -> hyper polarize cell + counteract sodium entering thru excitation synapse -> facilitating inhibition in the amygdala, hypothalamus, midbrain, and other areas Alcohol: Promotes the flow of chloride ions through the GABA receptor complex.
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What is the general adaptation syndrome (Selye's stress model)
1. Alarm stage: - release of hormones from adrenal stage - Activation of HPA axis 2. Resistance phase - decline of sympathetic response - cortisol and other hormones levels are still high - decrease activity to save energy 3. Exhaustion stage - occurs after prolonged stress - no longer have energy to sustain responses
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What happens when the hypothalamic-pituitary-adrenal (HPA) axis is activated?
When event is appraised stressful, hypothalamus stimulates pituitary gland to secrete adrenocorticotropic hormone (ACTH) -> ACTH stimulates adrenal cortex to release glucocorticoids, in particular cortisol -> mobilize energy storage and reduce inflammation - reacts more gradually vs sympathetic nervous system but continues as long there is stress
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What are leukocytes and types?
White blood cells B cells, T cells, Natural killer cell
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How do the leukocytes fight bacteria infection?
B cells -> secrete antibodies and "tag" cell -> will attack if tagged cell is unfamiliar, it attack + help in remembering intruder to build up anti body T cells - - Helper T cells: help B + other T cell to multiple - Cytotoxic T cells: directly attack particular intruder Natural killer cell - attack all intruders
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What is cytokines?
Released by leukocytes, small protein that combacts infections - trigger the release of prostaglandins that cross the blood–brain barrier and stimulate the hypothalamus to produce fever, sleepiness, lack of energy, lack of appetite, and loss of sex drive - too high of cytokines results in nasal congestion ect
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What is resilence
the ability to recover well from a traumatic experience -increases with strong social support, physical health, previous stressful experience
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How does prolonged stress affects our immune system?
Longer stress last, - greater risk of illness - produce symptoms to depression - increase release of cortisol -> enhanced metabolic activity throughout the body Neurons in hippocampus are more vulnerable to damage to toxins or over stimulation -> impaired memory
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What is lateralization?
the division of labor between the two hemispheres
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What is the corpus callosum?
the sets of axons that allow the left and right hemisphere exchange information
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What are the anatomical differences between the hemisphere?
One section of the temporal cortex, the planum temporale is larger in the left hemisphere than the right side
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What is split brain syndrome?
People with the corpus callosum cut -> can use two hands independently but struggle to use hands together
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What is Williams syndrome?
Most people with this condition have intellectual impairment - most have difficulty with attention, numbers and visuomotor skills
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What proves that we are biologically specialized for language?
FOXP2 gene regulates protein that promotes synapse formation in the cerebral cortex and basal ganglia E.g. FOXP2 gene from human differs from Chimpanzee Our motor cortex that controls vocal cords have greater connections to the rest of the cortex than in monkeys - greater connection = more complex and detailed control of sound production
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What is dyslexia?
impairment of reading by someone with adequate vision, motivation, cognitive skills, and educational opportunity - hearing problems BUT its impaired auditory memory, such as low accuracy at noting whether two sequences of tones, separated in time were the same or different -> brain handles auditory info funny
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What causes people to develop dyslexia?
Possible reason: area in temporal cortex called the visual word form area -> active in left hemisphere -> area becomes highly responsive to written words
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What is an antagonist drug?
Drug that blocks a neurotransmitter
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What is an agonist drug?
Drug that mimics or increases the effects of a neurotransmitter
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What is drug affinity and efficacy?
Affinity: drug able to bind to receptor and efficacy is tendency to activate said receptor A drug that binds to a receptor but fails to stimulate it has affinity but not efficacy
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What is the nucleus accumbens?
Brain reward centre where dopamine is released
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What are the features of an addiction?
Craving: insistent search of item - even prolonged abstinence, cues associated with habit can trigger a renewed craving Tolerance and withdrawal: increase tolerance to habit and need more for the same satisfaction withdrawal: when body expects drug, react strongly when drug is absent
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What is the genetic predisposition to alcohol abuse?
Gene that controls metabolism tf alcohol After drinking ethyl alcohol -> enzyme in liver metoablize it to acetaldehyde, a toxic substance -> Enzyme (acetaldehyde dehydrogenase) conveerts acetaldehyde to acetic acid, chemical used for energy People with less acetaldehyde dehydrogenase metablise acetaldehyde slowly -> drink too much and then accumulate acetaldehyde -> hangover
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What is Antabuse? How it work?
Help combat alcohol abuse Antagonize the enzyme that metabolizes acetaldehyde -> make you ill when you drink alcohol
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What is methadone?
A less harmful drug than heroin and morphine -> activates the same brain receptors and produce same effects but has advantage that it is taken orally -> slows the entering of blood and then to brain, avoid the "rush" that disrupts behavior - DOES not eliminate addiction -> cravings do return
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What is major depressive disorder?
Affective - diminished interest or pleasure - feeling sad and helpless - feeling worthless, guilt - recurrent thought of suicide Physical - fatigue, loss of energy - difficulty sleeping - weight loss or gain, decrease in appetite Cognitive - diminished ability to think or concentrate, indecisiveness Behavioural - psychomotor retardation or agitation
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What is the DSM-V diagnose criteria for major depressive disorder?
(Almost) every day for a minimum of 2 weeks, showing at least 5 or more symptoms One or more symptoms of - feeling sad and helpless (depressed mood) - diminished interest or pleasure Additional symptoms of -- feeling worthless, guilt - recurrent thought of suicide - fatigue, loss of energy - difficulty sleeping - weight loss or gain, decrease in appetite - diminished ability to think or concentrate, indecisiveness - psychomotor retardation or agitation
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How does genetics play a role in major depressive disorder?
Moderate degree of heritability - children of parents with depression are 3x likely of developing depression themselves Early vs Late onset - if your parents have depression before 30, you are more likely to develop depression - if you develop depression later in life, you have higher risk of vascular dementia -> causes the metabolism of the brain to be reduced
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How does environment and genes affect your chance of developing major depressive disorder?
- Effect of serotonin transporter gene depends on amount of stress -> The more you experience more stressful life events, the type of gene will affect how likely you develop depression
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What are the (biological) treatment for depression?
- Selective Serotonin Reuptake (SSRI): Block serotonin from binding to serotonin transporter protein - Serotonin norepinephrine reuptake inhibitors (SNRI): block reputake of both serotonin and norepinephrine - atypical antidepressants: miscellaneous category - some block re uptake of dopamine - MAO inhibitors: block MAO from breaking catecholamines and serotonine into inactive forms (MAO help breakdown the excess transmitters) - not popular, gotta avoid taking certain foods - tricyclic antidepressants: blocking transporter proteins that reabsorb serotonin, dopamine, and norepinephrine into the presynaptic neuron after their release
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How do antidepressants work?
The number of neurotransmitter is not different from depressed to non depressed persons - sudden decrease in serotonin does not lead to feelings of depression - one type is not better than the other - medication affect synapse within hours, effects is only noticeable after 2-4 weeks One hypothesis - depressed people tend to have a low brain reprieved neurotrophic factor (low BDNF) - show smaller hippocampus - reduced production of new hippocampal neurons - decreased learning capacity
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Are antidepressants effective?
We do see improvements of symptoms and reducing severity -> however, only those who have severe depression that gets treatment, improve considerably vs those who took placebo or with mild depression When people change antidepressants -> don't know if because they need the change or if they reached the max effect
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When do we use antidepressants or psychotherapy?
Dysthymia: long-term, lifelong condition of unhappy mood - antidepressants work better abuse/neglect during childhood: psychotherapy better - often you do both and allows the overlapping effects of antidepressants and psychotherapy - increased metabolism in same brain area - changing thoughts -> changes brain chemistry
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What is bipolar disorder?
alternate between depression and its opposite, mania. Mania is characterized by restless activity, excitement, excessive self-confidence, rambling speech, and loss of inhibitions. In depression-> low metabolic rates; In mania->high metabolic rates (shown in glucose usage in brain) Type 1: full fledged manic episodes Type 2: mild, hypomanic episode - usually has its onset in the teenage years or early 20s
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What is schizophrenia?
Disorder characterized by deteriorating ability to function in everyday for at least 6 months and at least two of following: +ve symptoms: - Hallucinations (auditive hallucinations most prevalent) - delusions: unjustifiable beliefs - disorganized speech - grossly disorganized behavior -ve symptoms: - weak or absent signs of emotion, speech and socialization CANNOT BE CAUSED BY ANOTHER DISORDER
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What is the genetic influence of developing schizophrenia?
MZ twins have 48% of developing - yet DZ twins have 17% chance while actual sibling is 9%, yet the genetic makeup of DZ twins have similar genetic makeup like siblings so why is it so much higher?
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What genes potentially increase your risk to schizophrenia?
Genes that control cell surface proteins that immune system recognizes DISC1(disrupted in schizophrenia 1): controls differentiation and migration of neurons, brain development, production of dendritic spines, generation of new neurons in hippocampus Microdeletion: loss of a small part of a chromosome
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What is the neurodevelopmental hypothesis? (Schizophrenia)
prenatal or neonatal difficulties—of either genetic or environmental origin—can produce abnormalities in the developing brain that predispose to schizophrenia - doroslateral prefrontal cortex as area often impaired in schizophrenia is often the slowest brain area to mature
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What is the two-hit hypothesis (schizophrenia)?
schizophrenia is a result of a combination of genetic predisposition and impacts from environment in prenatal/neonatal development, later in life or both
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What are the prenatal/perinatal/neonatal influences to developing schizophrenia?
intermediate risk factors - living in crowded city - pollution? - toxoplasma gondii (parasite) Low risk factors - poor nutrition of mother during pregnancy - extreme stress of mother during pregnancy - complications during delivery - premature birth - low birth weight - head injuries in early childhood Season of birth effect; viral infection more prone in summer so those who give birth in winter tend to be more prone to depression ect
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What kind of brain abnormalities do people with schizophrenia showcase?
- Less than average gray matter and white matter - Larger than normal ventricles - Smaller hippocampus - Abnormalities in the Dorsolateral prefrontal cortex (area that matures slowly)
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What are some antipsychotic drugs (dopamine) for schizophrenia?
Two chemical families - Phenothiazines: chlorpromazine - Butyrophenones: Haloperidol - each drug blocks dopamine synpase -> specifically type D2 receptors Dopamine-blocking antipsychotics relieve positive symptoms -But do not take away the cause - Side effects: tardive dyskinesia (tremors and other involuntary movements)
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What is the dopamine hypothesis for schizophrenia?
Schizophrenia results from excess activity at dopamine synapses in certain brain areas Evidence: - Effect antipsychotics -Substance-induced psychotic disorder -Schizophrenics seem to have twice as many D2 receptors occupied as normal
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What are the 2nd gen antipsychotics (atypical antipsychotics) for schizophrenia?
- relieve schizophrenic symptoms with less risk of movement problems - called clozapine and risperidone Have less effect on dopamine D2 receptors; more strongly antagonize serotonin type 5-HT2 receptors and increase the release of glutamate -More effective at treating the negative symptoms and are now more widely use
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What is the glutamate hypothesis of schizophrenia?
Schizophrenia is associated with lower release of glutamate and fewer than normal glutamate receptors in the prefrontal cortex Evidence: - Larger doses of PCP (which inhibits NMDA glutamate receptors)→ positive AND negative symptoms - In pre-adolescents: little if any psychotic response - In recovered patients → LONG-LASTING RELAPSE
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What is the characteristics describing autism spectrum disorder?
- Deficits in social and emotional exchange - Deficits in gestures, facial expressions, and other nonverbal communication - Stereotyped behaviors, such as repetitive movements - Resistance to a change in routine - Either weak or exaggerated responses to stimuli, such as indifference to pain, panicked reaction to a sound, or displeasure at being touched
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What are the possible causes to autism?
Rare de novo genetic mutations Difficulties in prenatal environment exposure to large amount of pollutants if your family have autoimmune disease you are at higher risk Eating folic acid (vit B) decreases risk