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PHGY314 > Chacron lectures 1-5 > Flashcards

Chacron lectures 1-5 Flashcards

1
Q

what brain areas are for motivation?

A

amygdala and hypothalamus

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2
Q

what is the basal ganglia involved in?

A

motor action

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3
Q

what brain area is for 3D coordination?

A

posterior parietal cortex

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4
Q

what is rostral vs caudal

A

rostral is towards the nose, caudal is towards the back of the brain

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5
Q

what is the brainstem made of?

A

midbrain, pons, medulla

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6
Q

name the major division of the central nervous system from dorsal to ventral

A

cerebral cortex
diencephalon
brainstem (midbrain, pons, medulla)
cerebellum (caudal to brainstem)
spinal cord

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7
Q

name the primary brain vesicles from most rostral to caudal.

A

prosencephalon (forebrain), mesencephalon (midbrain), rhombencephalon (hindbrain)

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8
Q

name the secondary brain vesicles of the forebrain

A

paired telencephalic vesicles, diencephalon, paired optic vesicles

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9
Q

in what secondary brain vesicle do the thalamus and hypothalamus evolve from?

A

diencephalon

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10
Q

what secondary brain vesicle do the olfactory bulbs emerge from?

A

telencephalon (telencephalic vesiles / cerebral hemispheres)

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11
Q

what “holes” are encapsulated in the telencephalon and diencephalon respectively?

A

lateral ventricles and the third ventricle

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12
Q

name 3 white matter structures found in the developed forebrain

A

corpus callosum, cortical white matter, internal capsule

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13
Q

what structures are found in the developed mesencephalon?

A

tectum and the tegmentum that contains the cerebral aqueduct

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14
Q

what is another name for the medulla?

A

myelecephalon

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15
Q

what is another name for the pons and cerebellum? what primary brain vesicle are they located in?

A

metencephalon, located in the rhombencephalon

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16
Q

name the structures in the hindbrain

A

metencephalon (pons and cerebellum), myelencephalon (medulla), encapsulate the fourth ventricle

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17
Q

what are the 3 steps of the neural tube development?

A
  1. 3 vesicles
  2. 5 vesicles
  3. 3 flexures
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18
Q

what are the 3 flexures of the neural tube? from rostral to caudal

A

cephalic, pontine, cervical flexure

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19
Q

Name 3 signaling molecules(morphogens).
what do they affect?

A

Shh (sonic hedgehog), BMP (Bone morphogenic proteins), Wnt (protein family).
They affect transcription factors

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20
Q

where are Wnt signaling vs inhibitors found? what genes do they control?

A

Wnt inhibitors are more rostral, Wnt signaling are more caudal
They control Otx2 and Gbx2 genes

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21
Q

Where are Otx2 vs Gbx2 genes found?

A

Otx2 rostrally (forebrain and midbrain), Gbx2 caudally (anterior hindbrain)

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22
Q

what are similarity and differences between a rat vs a human brain?

A

similarity: same overall structure
differences:
- rats don’t have sulcus or gyrus
- they have bigger olfactory bulbs
- no arc in their cerebral hemispheres
- different brainstem orientation

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23
Q

name the cerebral hemispheres

A

frontal, parietal, temporal, occipital

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24
Q

what is called the gyrus surrounding the corpus callosum?

A

cingulate gyrus

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25
Q

name the 3 sulci of the brain

A

central, lateral, cingulate

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26
Q

what does golgi stain for?

A

grey matter (cell bodies)

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27
Q

what does Weigert stain for?

A

white matter (axons)

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28
Q

name the 6 layers of the neocortex

A

1: molecular layer
2: external granule layer
3: external pyramidal layer
4: internal granule layer
5: internal pyramidal layer
6: multiform layer

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29
Q

what layer is largest in the primary visual cortex? why?

A

layer IV (4) because it receives input from thalamus

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30
Q

what layer of the PVC do feedback projections to the thalamus come from?

A

layer VI (6)

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31
Q

in the PVC, what are layer IV inputs and projections?

A
  • monocular inputs from thalamus (dLGN)
  • binocular projections to layers III and IVb of the visual cortex
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32
Q

where do layers II, III, and IVb in the PVC project to?

A

to other layers and areas of the visual cortex

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33
Q

in the PVC, where does layer V project to and what does it control?

A

project to pons and superior colliculus to control visually guided voluntary movements(subcortical areas)

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34
Q

in the PVC, where does layer VI project to?

A

it projects BACK to dLGN of the thalamus

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35
Q

what layer is largest in the primary motor cortex?

A

layer V (5) because it sends output info to subcortical structures including basal ganglia

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36
Q

as a general rule in the neocortex, where do ascending vs descending projections originate from / project to?

A
  • ascending originate in layers II and III and project to layer IV
  • descending projection originate in deep layers V, VI and project back to layers I, II, VI
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37
Q

what are chandelier cells?

A

inhibitory interneurons that terminate on axons of layer II and III pyramidal cells (prevents AP transmission)

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38
Q

what are basket cells?

A

inhibitory interneurons that terminate on cell bodies (soma) of pyramidal cells (prevents AP firing)

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39
Q

what are neurogliaform cells? what layer do they act in?

A

inhibitory interneurons that create axosomatic synapses on spiny non-pyramidal neurons of layer IV

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40
Q

describe ascending projection in visual cortex

A

V1 layer II & III -> V2/V3 layer IV

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41
Q

describe descending projection in visual cortex

A

V2/V3 layer V, VI -> V1 layers I, II, III

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42
Q

name the 3 main structures in the cerebral cortex

A
  1. Basal Ganglia
  2. Hippocampus
  3. Amygdala
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43
Q

how are structures in cerebral cortex (ex BG, hippocampus, amygdala) organized?

A

in nuclei instead of in layers

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44
Q

describe fast-spiking vs regular spiking neurons. give example for each.

A

fast spiking = short AP, high discharge rate (putative interneurons)
regular spiking = large AP (pyramidal neurons)

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45
Q

where do skin sensory receptor neurons relay information to?

A

to the dorsal column via the dorsal horn

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46
Q

where does the thalamus project to?

A

primary sensory cortical areas

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47
Q

name 3 thalamus nuclei and the system they are involved in?

A

lateral geniculate nucleus (visual)
medial geniculate nucleus (auditory)
ventral posterior lateral (vestibular)

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48
Q

name a thalamic subnuclei involved in motor control

A

ventrolateral nuclei

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49
Q

what do thalamic 2nd order sensory areas do?

A

change how primary nuclei respond to peripheral info (ex pulvinar nuclei)

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50
Q

how do peripheral vs central sensory neurons respond to stimulus?

A

peripheral: respond to most stimuli differently (dense code)
central: respond to specific stimuli (sparse code)

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51
Q

describe dense vs sparse code

A

Dense: all the neurons respond differentially
Sparse: only a small fraction of neurons respond respond to any given stimulus (metabolically more efficient)

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52
Q

what does information processing depend a LOT on?

A

context! and internal brain state

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53
Q

projection neurons respond to most stimuli, but is it in a random way?

A

not random, they all respond in different ways

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54
Q

what kind of activity can projection/peripheral neurons (like PN1 neurons in the example) show?

A

spontaneous activity

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55
Q

what is special about olfactory sensory pathway?

A

it goes straight from the olfactory bulb neurons to the anterior piriform cortex; doesn’t go through the thalamus

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56
Q

how do neurons in mouse anterior piriform cortex APC fire?

A

sparse coding: they fire to specific cells only (look at slide 12)

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57
Q

definition of feature invariance. explain

A

Neural representations become invariant to identity preserving transformations of behaviorally relevant stimulus features (neurons respond to object no matter the size, position, color)

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58
Q

give an example of how neurons can have selectivity (as opposed to invariance). what coding do they use?where can we find selective neurons?

A

they will only respond to a specific model of car of a specific color. they apply the “AND” operation. they are sparse coding.
- found in V4

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59
Q

what is the mcgurk effect?

A

auditory-visual illusion that illustrates how perceivers merge information for speech sounds across the senses (how brain integrates different stimuli)

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60
Q

the McGurk effect is the perfect example of what brain area working?

A

Multimodal cortex putting together multimodal information

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61
Q

where do the thalamus subnuclei project to?

A

to different unimodal (primary) cortex areas for each sense

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62
Q

explain the general sequence of cortical processing for the somatosensory system after the thalamus

A
  1. primary somatosensory (unimodal) cortex
  2. unimodal association cortices
  3. multimodal association cortices
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63
Q

simply describe the pathway for voluntary motor control?

A

corticospinal pathway: layer 5 (V) motor cortex neurons synapse on interneurons in the VENTRAL horn of the spinal cord. hose neurons cross the spinal cord at the medulla-spinal cordjunction

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64
Q

what other brain areas other than motor cortex send descending information for voluntary movement? (6)

A

thalamus, midbrain, red nucleus, pons, cerebellum, amygdala

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65
Q

what brain areas are involved in ascending pathways of voluntary control?

A

cerebellum, deep cerebellar nuclei, red nucleus, midbrain, thalamus ventrolateral nucleus, basal ganglia,

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66
Q

where is the extrapersonal space map located in the brain?

A

posterior parietal cortex

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67
Q

what is caused by lesions in posterior parietal cortex (extrapersonal map) (4)

A

visual neglect, personal neglect in reference to body, representational neglect, optic ataxia

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68
Q

what is optic ataxia?

A

difficulties reaching/grabbing objects in extrapersonal space

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69
Q

what regions did they identify to be involved in planning and control of voluntary movement via single unit (neurophysiological) recording?

A

parietal cortex regions MIP, VIP, LIP, DP (SPATIAL INFORMATION PROCESSING)

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70
Q

describe dorsal vs ventral stream

A

dorsal /parietal stream: for spatial information (where); projects to frontal association areas
ventral/temporal stream: for emotional significance (what); projects to ventral frontal cortex
- both go from back to front

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71
Q

what are frontal association areas involved in?

A

controlling motor functions that require spatial information

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72
Q

what are ventral regions of frontal cortex involved in?

A

identifying and assigning emotional significance to objects

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73
Q

what is object centered visual neglect?

A

only the side of the object opposit to the side of the lesion is neglected

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74
Q

someone with a unilateral lesion to the right posterior parietal cortex will be able to draw which side of an image properly?

A

he can draw the right side

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75
Q

visual neglect for objects due to a lesion is linked to the dorsal or ventral visual pathway?

A

dorsal visual pathway

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76
Q

what did damage to the right posterior parietal cortex cause related to landmarks?

A

patient could only recall landmarks to their right (not the landmarks on the opposite side of lesion)

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77
Q

what is personal neglect caused by right posterior parietal cortex lesions?

A

patient can only draw a self portrait of the right side of their face (can’t draw the side opposite to lesion)

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78
Q

more specifically what region of the parietal cortex is affect in people with optic ataxia?

A

posterior (in ex, it was dorsomedial) parietal cortex, where extrapersonal space is represented

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79
Q

what did lesions of parietal cortex in monkeys cause?

A

spatial motor and spatial perceptual deficits comparable to those in human, and difficulty directing eye movements towards objects in opposite hemispace

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80
Q

what are VIP, MIP, LIP, AIP regions of parietal cortex involved in?

A

transforming sensory inputs to motor outputs

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81
Q

single unit recordings of LIP neuron showed what?

A

Retinal Centered Coding of Visual Target, but attention specific

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82
Q

what is declarative/explicit memory? what brain areas are involved?

A

facts/events
hippocampus-medial, temporal lobe, diencephalon

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83
Q

what are the 4 types of nondeclarative/implicit memory? what brains areas are involved?

A
  • skills/habits: Striatum (BG), motorcortex, cerebellum
  • priming: neocortex
  • basic associative learning: emotional response (amygdala) and skeletal musculature (cerebellum)
  • nonassociative learning: reflex pathways
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84
Q

what is associative vs non-associative learning?

A

basic associative learning:
- emotional response: amygdala
- skeletal musculature: cerebellum
non-associative learning: reflex pathways

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85
Q

what surrounds the hippocampus?

A

perirhinal cortex, entorhinal cortex, parahippocampal cortex

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86
Q

what are the regions of the hippocampus and what links them? what cell types do they have?

A

dentate gyrus (granule cells) - mossy fiber connections -> Ca3 (pyramidal) - Schaffer collaterals -> CA1 (pyramidal) -> subiculum

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87
Q

what do lesions of the right vs left hippocampus affect?

A

right = spatial memory
left = words, objects people

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88
Q

what is special about taxi driver’s brain?

A

they have a bigger posterior hippocampus and a smaller anterior hippocampus than average

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89
Q

what process in the hippocampus is thought to underly the formation of new memories?

A

neurogenesis

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90
Q

what 3 things are necessary for spatial learning

A

internal compass, external landmarks, neural representation of our environment

91
Q

how did different hippocampal lesions affect rat’s memory of where the platform is in a water maze? (similar to humans)

A

CA3 lesion decreases the spatial accuracy (could still find platform but took longer)
complete hippo lesion: no spatial accuracy (can’t find platform)

92
Q

what different about rodent’s hippocampus?

A

it is banana shaped lol

93
Q

how is labeled line code applied to CA1 pyramidal cells?

A

their firing is location dependent

94
Q

do CA1 place field neurons have directional selectivity?

A

no

95
Q

did they find topographic organization in place field neurons?

A

no: no relationship between CA1 neurons proximity and their place field position

96
Q

why is it important for place fields to be stable over time?

A

important for memory retention of an environment

97
Q

what feature of Ca1 pyramidal cell ensures coding of place or location?

A

omnidirectionality (allowscoding of place/location independently of head direction)

98
Q

what were the results from the experiment of rotating rat’s environment with vs without the animal’s knowledge?

A
  • rotation of place field did occur when the animal was not aware of the rotation
  • rotation of place field did NOT occur when the animal WAS aware or the rotation
99
Q

what did they conclude from the rotation rat’s environment experience?

A

place fields are determined by EXTERNAL landmarks when they don’t contradict the internal cues.
When there is contradiction, internal cues dominate.

100
Q

does remapping of place field happen when the environment is “translated”

A

no

101
Q

does isotropic scaling change of environment cause place field remapping?

A

no; place fields are largely insensitive

102
Q

Are place fields sensitive to novelties in ​the environment?​

A

yes but only when the novelty or removal happens inside the place field

103
Q

can you predict the effect of changing a complex environment (moving distal and proximal cues) on place fields? what happens to the place fields?

A

no;
some place fields follow distal cues
some place field follow proximal cues
some place fields completely remapped

104
Q

what happened to the place field of a rat’s neurons after a few laps in a unidimensional environment?

A

the place field becomes wider in the direction that the rat is coming from

105
Q

what explains the widening of the place field in rats doing unidimensional laps?

A

because the neurons receive stronger synaptic input which strengthen the synaptic connection as the rat gets used to the environment

106
Q

what did they use in epilepsy patients to locate the seizure focus?

A

single neuron recordings and intracranial electrodes

107
Q

what did they find in epileptic patients who played the taxi driver game?

A

place sensitive neurons

108
Q

name 3 characteristics of the place sensitive neurons found in humans

A
  • they cover most of the environment
  • they are not directionally selective
  • there are fewer than in rats
109
Q

place cells make up what % of the hippocampus in humans vs rats?

A

24% in humans vs 80% in rats

110
Q

what is the caveat of testing place cells in humans that make the results less accurate?

A

the patient were immobile and used virtual reality

111
Q

what type of cells for location were found in non-human primates?

A

GAZE cells in hippocampus with a 3D place field

112
Q

what is a limitation of using rodents compared to humans?

A

they use olfaction so much more than vision

113
Q

what is Hebb’s postulate?

A

cells that fire together, wire together

114
Q

what underlies associative (Hebbian) plasticity?

A

correlation between pre- and post- synaptic activity

115
Q

what is the protocol for inducing plasticity that they used?

A

stimulating a Schaffer collateral with tetanus of specific frequencies

116
Q

what Hz of tetanus induces LTD vs LTP?

A

1 Hz induces LTD,
50 Hz induces LTP

117
Q

what happens to post-synaptic neurons receiving 10 Hz tetanus?

A

EPSP goes back to normal

118
Q

what ion usually blocks NMDA receptors at resting membrane potential?

A

Mg2+

119
Q

how can MG2+ be removed to stop blocking NMDA receptors?

A

by strong postsynaptic depolarization causing GLUTAMATE to bind NMDAr

120
Q

what happens when Mg2+ stops blocking NMDAr?

A

Na+ and Ca2+ enter the post-synaptic cell, and K+ exits the cell via NMDA

121
Q

what kind of receptors and ions can cause associative plasticity?

A

NMDA receptors and calcium ions

122
Q

at what levels of NMDA and Ca2+ do we see LTD or LTP?

A
  • low/moderate NMDA activation and Ca2+ flow = LTD
  • high NMDA activation and Ca2+ flow = LTP
123
Q

why are LTD and LTP opposing mechanisms?

A

one makes the synapse stronger, the other makes the synapse weaker

124
Q

What is APV?

A

substance that blocks NMDAr

125
Q

what is EGTA?

A

a calcium chelator (calcium buffer)

126
Q

what happens to LTP when they give moderate vs high APV to neurons?

A

moderate APV changes LTP to LTD.
high APV completely cancels the effect of the tetanus.

127
Q

the effect of APV on LTP show that it affects NMDArs in what way?

A

APV deactivate NMDAr which usually contribute to LTP

128
Q

what happens to LTP when they give moderate vs high EGTA to neurons?

A

moderate EGTA: LTP -> LTD
high EGTA: no effects of tetanus

129
Q

what does the effect of EGTA on LTP show?

A

calcium is required for LTP

130
Q

the APV and EGTA experiment show what?

A

plasticity required calcium entry via NMDAr

131
Q

why does moderate CA2+ cause LTD

A

moderate CA2+ in synaptic cleft moderately activates NMDAr and interact with protein phosphatases in the post-syaptic cell that have high affinity for calcium

132
Q

how does high Ca2+ cause LTP?

A

high Ca2+ strongly activates NMDAr and saturates protein phosphatases. It interacts with Protein kinase C and calmodulin kinase II, ausing LTP

133
Q

remember _____ tetanus freq causes LTP, ____ tetanus freq causes LTD

A

high
low

134
Q

what characteristic of protein phosphatase causes LTD?

A

high affinity to Ca2+ (binds Ca2+ at low conc)

135
Q

what happens to rat in the water maze who were given APV?

A

they couldn’t remember where the platform was (no more spatial memory)

136
Q

what are AMPA receptors permeable to?

A

NA+ & K-

137
Q

KO of LTP causes what?

A

no retention of place fields (but they can still form place fields)

138
Q

explain STDP spike timing dependent plasticity

A
  • if pre-synaptic cell fire before post = strengthening of the synapse
  • if post- before pre- = weakening of the synapse
139
Q

STDP can predict the _______ of place fields

A

shifting (?)

140
Q

intracellular recordings from mammalian ​
hippocampus showed similar properties what kind of neurons?

A

motorneurons

141
Q

in what kind of animals is implicit memory most easily studied? why?

A

invertebrates; it requires simple behavior, well understood anatomy

142
Q

what is special characteristic about aplysia californica?

A

Gill withdrawal reflex

143
Q

what is aplysia californica?

A

slow moving gastropod mollusk​

144
Q

how many neurons in aplysia vs average person?

A

~20000 in aplysia,
~10^11 neurons in humans

145
Q

aplysia can habituate to what kind of stimulus?

A

to harmless repeated stimuli (siphon touch)

146
Q

what stimulus causes dishabituation to siphon touch?

A

harmful stimuli (tail shock)

147
Q

name the 5 ganglions found in Aplysia

A

buccal, cerebral, pleural, pedal, abdominal

148
Q

aplysia neurons are big. what does this allow?

A

to identify the same individual pyramidal cells in different aplysia

149
Q

explain the simplified anatomy of aplysia nervous system

A

sensory neuron LE -> excitatory / inhibitory interneurons -> L7 motor neuron in gill

150
Q

what causes the SHORT TERM habituation (decrease post-synaptic response in motor neurons to siphon touch)

A

the decrease of releasable pool of vesicles at that active zone

151
Q

what causes the LONG TERM habituation?

A

decreased number of synaptic connections

152
Q

what happens to sensory vs motor neuron EPSPs during habituation?

A

sensory neuron EPSP stay the same;
motor neuron EPSP disappears

153
Q

what kind of interneuron is involved in in the facilitation of the gill withdrawal by tail shock​?

A

modulatory interneuron

154
Q

where does the modulatory interneuron from the tail synapse?

A

it synapses on PRESYNAPTIC TERMINAL of regular interneuron and of gill motor neuron

155
Q

how can short vs long term SENSITIZATION be achieved?

A

more tail shocks = longer sensitization (the longer aplysia responds to siphon touch)
- few tail shocks = short-term
- many tail shocks = long term

156
Q

what mechanism mediated by what neurotransmitter governs sensitization in aplysia?

A

synaptic facilitation mediated by serotonin 5HT

157
Q

what neuron releases serotonin? onto what neuron?

A

the faciliatory interneuron releases serotonin on the presynaptic terminal of the sensory neuron

158
Q

explain the cascade of event in a synapse for short-term facilitation by serotonin

A

serotonin in released from interneuron -> binds serotonin R -> G-protein bind adenylyl cyclase -> cAMP -> PKA
2 options:
1. PKA catalytic subunits close K+ channel, open Na2+ channel to increase depolarization
2. PKA regulatory subunits
BOTH work to increase glutamate release onto the motor neuron

159
Q

how does long term facilitation work in aplysia?

A

the signal from the facilitatory interneuron goes to the nucleus of the sensory neuron where Ub hydrolase causes formation of new vesicles and new synaptic connection

160
Q

when does long term facilitation happens?

A

when LTP is maintained for a long time

161
Q

name the 3 basics that are common to aplysia and humans?

A
  1. plasticity requires calcium
  2. cell signaling i modulated by neuromodulator (serotonin vs dopamine)
  3. long term plasticity requires signaling to the nucleus
162
Q

plasticity in what region of the hippocampus requires NMDAR and Ca2+?

A

in CA1

163
Q

what are the pre and post-synaptic mechanisms of plasticity that are similar across species

A
  • Pre: increase/decrease in vesicle pool​
  • Post: insertion/deletion of AMPAR, number of synaptic boutons
164
Q

Exposure to what? early in development is critical for vocal learning

A

vocalizations

165
Q

does language develop spontaneously?

A

yes!

166
Q

what is a spectrograph?

A

graph of time varying frequency spectrum. we can see human speech with it

167
Q

what are the 3 phrases of a songbird song?

A

whistle, trill, buzz

168
Q

how long is songbird’s listening and practice phase (before crystallization)?

A

90 days

169
Q

what are the 3 phases of song learning?

A

listening, practice, crystallization

170
Q

in humans and songbirds, what does a loss of feedback cause?

A

gradual deterioration of speech

171
Q

do birds have accents?

A

yes they have region specific song motifs

172
Q

in songbirds, what is required for the normal song?

A

social interaction and auditory feedback

173
Q

during the first 10 months of life, what kind of speech do humans produced?

A

universal speech, no matter the language

174
Q

during the first 8 months of life, what kind of speech do humans percieve?

A

universal speech

175
Q

birds are born with ______-_________ predispositions

A

species-specific

176
Q

isolated WCS can sing spontaneously, but their song is ____ ________

A

not attractive

177
Q

how is song learning “creative”?

A

if a bird is tutored 2 different songs model, it will mix both to create its own song

178
Q

what happens if a WCS is thought the song backwards? (inversed syllable order)

A

WCS can sing the sequence backwards

179
Q

explain the 3 steps of the error-driven model for learning and maintaining song

A
  1. storage of a model/template (syllable and sequence) of the song
  2. bird sings and tries to reproduce
  3. song feedback/comparison
180
Q

name the 3 brain areas involved in song production

A

HVC -> RA -> nXIIts

181
Q

what is bird’s vocal organ?

A

Syrinx

182
Q

name the 3 brain areas involved in song production?

A

LMAN, Area X, DLM

183
Q

what are the effects of area x lesions in juveniles vs in adults?

A

juvenile = disrupt song learning
adults = no effect

184
Q

what brain areas were paired in the LTP experiment in songbirds

A

HVC + LMAN -> Area X

185
Q

what does it mean that the plasticity in the LTP experiment is synapse specific and activity dependent?

A

giving tetanus to LMAN axon will potentiate the LMAN -> AreaX synpase, but not the HVC -> AreaX synapse

186
Q

how did the prof’s experiment indicate that LTP induction at these synapses may be described by the Hebbian rule (cells that fire together, wire together)

A

High-frequency tetanus alone or depolarization alone failed to induce LTP; LTP requires both pre- and postsynaptic activity

187
Q

what can we conclude if LTP induction after pairing in area X is blocked by APV and BAPTA?

A

Similar to the classic LTP in hippocampus, the LTP induction in area X is dependent on Ca2+ and NMDAr

188
Q

is the % change of EPSC high in adult or juvenile birds? why?

A

higher in juvenile birds because they have more LTP because they are song learning

189
Q

what is the definition of sensory reafference?

A

how to distinguish self-generated vs external sensory input

190
Q

what is a reafferent stimulus?

A

stimulus from your brain

191
Q

what is an exafferent stimulus?

A

externally generated stimulus

192
Q

how do we distinguish exafferance vs reafference stimulus?

A

the system compares the actual afference to the copy element

193
Q

movements can lead to what type of stimulus?

A

sensory reafference

194
Q

what 2 stimulus are combined to give rise to a perceived stimulus?

A

efference copy + reafferent stimulus

195
Q

in the mechanical tickling experiment, what was the motor command, the reafference stimulus, and the perceived stimulus?

A

motor command = arm movement
reafference stimulus = tactile stimulus
perceived stimulus = tickling sensation

196
Q

what is the sensory discrepancy in the mechanical tickling experiment?

A

feeling caused by time delay between the efference copy and the actual sensory feedback

197
Q

what is the efference copy

A

predicted sensory feedback

198
Q

what is caused by a sensory discrepancy?

A

tickle

199
Q

what kind of information does the efference copy contain?

A

temporal and spatial information about the reafferent stimulus

200
Q

what did they train the bunny to do with the tone and air puff?

A

to start closing its eyes when it hears the tone, that always played before the air puff

201
Q

what happens to bunny with cerebellar lesion?

A

it can only blinks when air puff, not during the tone
(it forgets the association of air puff and tone)

202
Q

what is the cerebellum involved in?

A

balance, coordinating movement, timing of movement, timing of discontinuous movements, motor learning

203
Q

what is the most anatomically conserved structures throughout evolution?

A

cerebellum

204
Q

name the cerebellar layers from outer to inner and what is in them

A
  • molecular layer: parallel fibers
  • purkinje cell layer: purinje cells
  • granule cell layer: granule cell, climbing fibers, mossy fibers
  • white matter
205
Q

what happens if you co-activate parallel fibers and climbing fibers at the same time in the cerebellum?

A

LTD

206
Q

against what theory does the co-activation of parallel and climbing fibers causing LTD goes? why?

A

hebb’s postulate!
Hebb’s postulate says that this should give LTP, but in the cerebellum it gives LTD

207
Q

what happens to a patient wearing prism lenses that has impaired adaptation capacities? (inferior olive hypertrophy)

A

they can not get used to wearing the lenses and will keep throwing off target

208
Q

does sensorimotor coordination and adaptation to novel conditions required cerebellar function?

A
  • Sensorimotor coordination does not require the cerebellum.
  • Adaptation to novel conditions does require cerebellar function
209
Q

what kind of process is adaptation?

A

error driven process

210
Q

cerebellar LTD help achieve what?

A

cancellation of expected stimuli

211
Q

what is the weakly electric fish?

A

Electric fish that emits electric field through an electric organ in their tail

212
Q

what is special about the cerebellum of electric fish?

A

it is very developed (but has the same similar anatomy conserved across vertebrates)

213
Q

how do electric fish interact with their environment?

A

use perturbations of their self-generated electric field (electric organ discharge)

214
Q

what are electric fish;s reafferent stimulus with their EOD?

A

activation of their own electrosensory system via their EOD

215
Q

what are electric fish’s cerebellar layers?

A

granule layer, molecular layer, principal cell layer, sensory input layer

216
Q

what happens to a cerebellar neuron of electric fish when there is only the EOD?

A

it fires normally (moderate)

217
Q

what happens to a cerebellar neuron of electric fish when it is paired with an excitatory stimulus?

A

neuron fires a lot in response to the increase sensory input

218
Q

what happens to a cerebellar neuron of electric fish once you stop the excitatory stimulus?

A

activity goes does lower than before

219
Q

what happens to a cerebellar neuron of electric fish when the EOD is paired with an inhibitory stimulus?

A

opposite than excitatory stimulus

220
Q

do changes in the reafferent stimulus cause changes in the efference copy?

A

yes

221
Q

what underlies the adaptive cancellation of reafferent input?

A

anti-hebbian STDP

222
Q

what is anti-hebian STDP?

A

pre-synaptic EPSP followed by post-synaptic EPSP causes depression instead of activation

223
Q

where is anti-hebbian STDP found (what cells) vs hebbian STDP?

A

anti-hebbian = cerebellum (granule cell -< parallel fiber)
hebbian STDP = hippocampus

224
Q

maybe go over the last part of lecture with the graphs

A

PHGY314 (9 decks)

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