Phgy 314 Exam

Front 1

light adaptation (explain how molecularly, photoreceptors are able to change their dynamic range)

Back 1

after initial hyperpolarization, cGMP levels begin to raise again because you've got synthesis in the cell from transducin (GTP > cGMP) and this opens the Na channels again, depolarizing the photoreceptor. But it takes time for this cGMP to build up.

Now to hyperpolarize again, you're gonna have to increase the amount of light from the new steady state.

Front 2

Cones and rods vs. Parvo and Magno ganglion cells

Back 2

Not analagous:

Cones - high spatial and temp resolution
Parvo - high spatial, LOW temp resolution

Rods - low spatial and temp resolution
Magno - low spatial, HIGH temp resolution

Front 3

temporal frequency sensitivity

Back 3

ability to see gratings flicker at different rates

Front 4

equation for velocity of a drifting sinewave grating

Back 4

v = temp freq/spatial freq

Front 5

effects of magno vs. parvo lesions (in LGN)

Back 5

magno lesions:
- reduced ability to see movement

parvo lesion:
reduced ability to see things changing at low velocities
reduced ability to see high spatial freq
eliminated colour perception

Front 6

LGN synpase to superior colliculus

Back 6

for processing of eye position (source of creates blindsight (subconscious vision) when V1 is lesioned)

Front 7

cortical magnification factor

Back 7

further away from fovea, the less you are represented in V1

Front 8

cortical layers (function of cells in each layer)

Back 8

1-3 - output to inter-cortical connections
4 - input to cortex
5- output to motor neurons/subcortex
6 - output feedback to thalamus

Front 9

simple cells info vs. complex cells info

Back 9

simple cells
- info about orientation (some, 20%)
- info about contrast (on/off regions)

complex cells
-info about orientation
- no info about contrast (no on/off regions)
- built from integrating many simple cells

Front 10

complex cell model

Back 10

adds simple cells with on/off + off/on of same orientation

Front 11

hyper column (significance and makeup)

Back 11

x dimension - a L and R ODC
z dimension - all orientations of simple cell
y dimension - layers 1-6

significance: represents everything going on at 1 spot in your visual field (all columns have same RF in visual space)

Front 12

which layers do ocular dominance colmns exist in??

Back 12

only 4, the other layers are binocularly integrated

Front 13

blobs

Back 13

layer 2-3
doule opponent colour cells
connected to similar blobs through lateral connections

Front 14

latency (for motion selectivity) depends on:

Back 14

size of cell
number of inputs to a cell
biophysical properties of a cell

Front 15

depth cues

Back 15

perspective
background knowledge
binocular disparity

Front 16

what orientation do binocular disp. tuned cells prefer??

Back 16

vertical (vertical lines change most in humans cause our eyes are horizontally offset)

Front 17

contour integration cell model

Back 17

stim are too small for RF and orient nicely in line with other small stimuli but dont form full lines

-excitatory lateral connections

Front 18

contour

Back 18

lines that don't actually exist but are formed by patterns

Front 19

illusory contour detection (where? why?)

Back 19

V2 does it,

for seeing depth/texture in natural world (ie. river snaking through landscape)

Front 20

angle detection (where? why?)

Back 20

V2

to process shape and depth

Front 21

organization of MT

Back 21

(loose)
x axis - gradual shifting in motion orientation columns
z axis - areas of binocular disparity (near/far)

Front 22

effect of MT lesion

Back 22

cant see motion in NOISY stimuli (random dot coherence test)

Front 23

effects of V4 lesions

Back 23

cant filter out NOISY stimuli (similar spatial freq) when doing a spatial task (detecting slight tilt in spatial grating)

Front 24

complex shape & face detection (where? how?)

Back 24

TEO (IT)
requires integration of V4 receptive fields

Front 25

integration of form & motion (where? how? why?)

Back 25

- STPa (superior temporal parietal area)
- look for congruency in detail (vental stream) and motion (dorsal stream)
- very impt for biological motion (we are so sensitive to biological motion)

Front 26

why does mona lisa get ur attn looking elsewhere??

Back 26

low spatial freqs in smile are best picked up by peripheral ganglion cells (magno)

Front 27

optimal spatial freq for V1 neurons is?

Back 27

1-5 cycles per degree of visual field

Front 28

information threory/theory of visual system

Back 28

optimal (actual) code has minimal redundancy

Front 29

redundancy regulated by attention/salience

Back 29

keep redundant information (low spatial/low temp frequency) if there is attn directed at it or it is very salient

Front 30

power spectrum (explain the grid)

Back 30

y axis - amplitude of wave (intensity)
further from origin - higher spatial frequency
angle formed with x axis - orientation info

Front 31

ductus reunions

Back 31

connects aud/vestibular systems phsyically, reason why sometimes loud sounds make you dizzy

Front 32

labyrinth (location, composition)

Back 32

in petrous part of temporal bone
the otoliths + the canals in vestibular system, - fluid is continuous with scala media
- oldest part of inner ear

Front 33

macula

Back 33

sensory surface in the otoliths

Front 34

ampula

Back 34

sensory surface in the canals

Front 35

kinocilium (what, for who, function)

Back 35

- tall bulb thing taller than hair fibres
- for frogs and other species, humans dont have them
- unknown

Front 36

regular afferents vs. irregular afferents

Back 36

regular afferents
- innervate type 2 hair cells
- regular firing rates

irregular
- transient (quick to change), irregular firing
-faster response
- type 1 hair cells
- eveolved to deal with out of water probably (need balance more)

Front 37

striola (utrical vs. saccule)

Back 37

part of the macular surface where the kinocilium of cells face each other in utricle

kincilium face away from each other at this point in saccule

Front 38

otoliths vs. canals

Back 38

sensory organs for linear accn and gravity

sensory organs for angular accn, but mostly velocity during everyday head movements cus we dont move fast enough

Front 39

cristae/cupula (what, where)

Back 39

are parts of the ampula (sensory surfaces in canal)

- cristae - hair cells in ampula
- cupula - membrane (water tight) around ampula

Front 40

difference in receptor cells in otoliths and canals (2)

Back 40

1. cilia are much longer in canals
2. all hair cells oriented the same direction in each ampula

Front 41

the vestbular ocular reflex (function, phases, mechanism, timing)

Back 41

- to stabilize gaze during movement

- slow phase: to keep the eyes moving opposite the diretion of head turning
- quick phase: to reorient (with a saccade) your eyes (same direction as movement)

activated by triggering of canal hair cells
3 neuron arch:
1. vestibular afferents
2. central vestibular neurons
3. extraocular motor neurons

- 5ms (one of fastest movements in body)

Front 42

Ewald's first law

Back 42

stimulating a semicicular canal creates eye moments in that plane

Front 43

lesions to vestibular system (how to detect?)

Back 43

abnormal nystagmus (eye movement)

Front 44

caloric test (for what? tells u what?)

Back 44

- function of vestibular canals
- put warm fluid in the ear, the convection currents hopefully reach middle ear (hosizontal canals bulge into there), and then measure nystagmus from excitation

Front 45

halmagyi maneuver

Back 45

thrust head quickly, see if there is lag between saccade back to centre or not

Front 46

benign paroyxsmal positional vertigo

Back 46

- caused by stones from otoliths falling off the macula and into posterior canal,
-50% of old ppl have it at least once

Front 47

epley maneuver

Back 47

series of positional adjustments to get stones from macula back out of canals

Front 48

limitations of vestibular system (2)

Back 48

1. limited freq. of vestibular operation: lower freq than .1Hz (ie. on boat can give us poor sense of motion), and we adapt to moving at a a certain velocity after a while
2. - combination of gravity and linear accn (when flying a plane, deceleration + gravity = pitch down cause we think resultant is gravity)

Front 49

what makes movement difficult

Back 49

1) muscle generates unpredictable force (depends on length, and muscles are always diff lengths)

2) velocity of muscle contraction depends on external load (more load, slower velocity)

3) muscles create less force as they fatigue

Front 50

alpha motor neuron vs. gamma motor neurons

Back 50

alpha innervate extrafusal
gamma innervate intrafusal (spindles)

Front 51

muscle spindles (3 types, their [afferents], their {efferents}, functions (2))

Back 51

- to monitor spindle length and limb positions

nuclear bag fibres (b1 dynamic) [Ia] {gamma dynamic}
nuclear bag fibres (b2 static) [Ia, II] {gamma static}
nuclear chain fibres [1a, II] {gamma static}

Front 52

dynamic response vs. static response

Back 52

- the response of an afferent during muscle stretch (info about rate of stretch given)

- repsonse of an afferent after muscle stretch (info about length given)

Front 53

static gamma fibres (function, where, mechanism) vs. dynamic gamma fibres

Back 53

- increase the static response of afferents to muscle length
- influence the Ia afferents on b2 nuclear bags and nuclear chain spindles

dynamic
- increase firing of afferents during stretch (signal rate of stretch)
- impact Ia afferents on b1 (dynamic nuclear bag fibres)

both do this by contracting muscle spindles contractile component)

Front 54

types of extrafusal muscle fibres (3) (amounts in people)

Back 54

type I: slow contracting
dont get tired (in legs of long distance runner)

type II: fast contracting (weight lifter/sprinter has equal amounts of these)
IIa: fatigue resistant (to 50mins)
IIx: easily fatigued (1min)

Front 55

tetanic stimulation

Back 55

constant stim of motor neurons

Front 56

increase in muscle force is done by (2) mechanisms

Back 56

1) more motor neurons recruited
2) more APs fired by each neurons

Front 57

spike triggered averaging

Back 57

tells you how much a specific motorneuron is contributing to force:

later activated = more force = more APs

Front 58

golgi tendon (function, their afferents, firing mechanism)

Back 58

to measure force output by the muscle
use ib afferents to the brain to record this (squeezed by collagen fibres, increase in firing rate linear with force produced by muscle)

Front 59

impact of muscle spindles and gogli tendons on alpha motor neurons (reflex)

Back 59

muscle spindle afferents:
-increase activity of alpha motor neurons

golgi tendon afferents:
-decrease activity of alpha motor neurons (through inhibitory interneurons)

Front 60

monosynaptic stretch reflex impact on muscle spindle

Back 60

- alpha activation unstretches the muscle spindles (since the extrafusal is doing the contracting now)
- gamma motorneurons can then reset the spindle (so a1s fire during the muscle contraction)

Front 61

autogenic inhibition circuit (function, modulation)

Back 61

golgi - 1b - inhibitory interneuron - alpha motor neuron

function is to stop the excessive use of force, maintain constant force, and treat internal/external loads diff.

modulation: red nucleus, motor cortex, brain stem and is done to inhibit extensors at rest, etc. depends on behavioural state

Front 62

what causes time delay of reflex loop pathways (30ms of involuntary)?

Back 62

- the voluntary response (ie. if you want to cancel the reflex needs to come from cortex, so it takes time to get there and bac (long latency pathway))

Front 63

long latency issues (causes (2))

Back 63

- brainstem damage
- Parkinsons disease

Front 64

vestibularspinal reflex (pathway)

Back 64

- afferent > vestibular neuron > vestibular signals

Front 65

how vision contributes to sense of movement

Back 65

linear vection
the feeling of movement from being in a flowfield (can create postural effects)

Front 66

how vision contributes to balance/orientation

Back 66

- tilting/rotating of a visual field
- especially impactful when you cant rely on vestibular cues (ie. after a flight/being in space)

Front 67

how touch contributes to postural stability

Back 67

- light touch can help balance
- can be used when proprioceptive/vestibular function is abnormal (electronic tactile vest) match vest size with accelerometers

Front 68

reafference vs. exafference

Back 68

a movement you're doing on purpose

a movement you're not expecting to do

Front 69

computing sensory reafference

Back 69

sensor info - efference copy = exafference

efference copy made during planned motor command, it is minused from total afference when returning to the brain
- this way exafference that creates afference is what your brain calculates during expected movements (the efference copy cancels the afference signal form planned movement)

Front 70

some neurons record exafference only (where?)

Back 70

early vestibular processing

Front 71

gain fields in cerebellum

Back 71

cells that respond to rotation only when head is at a specific angle relative to body

Front 72

optic ataxia

Back 72

lesion in parietal lobe, reaching/orientation errors in contralateral visual field

Front 73

object centred neglect (damage where? how to relieve?)

Back 73

lesion in posterior parietal lobe (right hemisphere)
if you can recentre head relative to body or eyes relative to body

Front 74

lesions of parietal cortex create deficits (3)

Back 74

spatial motor deficits
spatial perceptual deficits
difficulty directing eye movements

Front 75

area LIP (function, reference frame, mechanism)

Back 75

- keeps eye-centred memory traces:
1. where stim was on retina,
2. how much the eye moved (done by efference copy)

eye-centered

Front 76

area VIP (function, reference frame, experiment with optic flow fields)

Back 76

- cells are body/head centered
- cells integrate touch and vision: touch top of head they fire and also signal top of visual field gets activated
- flow fields here are head centered:
> tuning for left/centre/right headings exist
> left and right pursuit did not change heading angle recorded by cells
> compensation for retinal smooth pursuit was done by efference copy of motor command

Front 77

spatial representation in premotor cortex (reference frame)

Back 77

- head-centered
- visual fields gander response relative to head, not retina

Front 78

spatial representation in prefrontal cortex (reference frame, function)

Back 78

- head centered
- lesions cause disruption of working memory in right half of space

Front 79

FAC (function, spatial reference frame)

Back 79

- has neurons that fire during delay part of working memory tasks
- neurons response to a certain location in space as well (head centered)

Front 80

how do head centered cells build sensitivity?

Back 80

- integrating vestibular/proprioceptive info (to know our head position)

Front 81

medial temporal lobe association area role in spatial cognition

Back 81

- spatial memory
- place cells in rats

Front 82

the three motor nuclei

Back 82

6- abducens - lateral rectus (pons)
4- tochlear - superior oblique (tegmentum)
3- oculomotor - the 4 other muscles (tegmentum)

Front 83

for lateral rectus saccade circuit: ocular motorneurons (what the firing codes, where they are)

Back 83

velocity of movement (pulse, AP bursts), final position (sustained firing)

They are from abducens (pons) to eye

Front 84

for lateral rectus saccade circuit: burst neuron (what the firing codes, where they are)

Back 84

fire during change in eye position parapontine reticular formation (innervate the abducens)

Front 85

for lateral rectus saccade circuit: omnipause neuron (what the firing codes, where they are)

Back 85

fire during fixation (doesn't matter what position), inhibit burst neurons in PPRF

in raphe nuclei (connect to PPRF)

Front 86

tonic neuron

Back 86

fire to indicate position only (do not measure change), keeping the muscles in the same place

in prepositus (connect to abducens)

Front 87

for saccade circuit: superior colliculus (what the firing codes, inputs)

Back 87

controls whether omnipause or burst neurons are excited
- you decide to make a saccade in the superior colliculus

- FEFs, PPC, substantia nigra, basal ganglia

Front 88

vestibular ocular reflex pathway

Back 88

- 5-6ms
- canals > vestibular nuclei > abducens > eye muscles

Front 89

decibel system (why we use it, how to calculate)

Back 89

to make linear the relationship between perceived loudness and units

I = 20log(P/Pstd)

Front 90

resonant frequency of meatus

Back 90

2000-5000Hz

Front 91

amplification by the middle ear (mechanisms and amounts), resonant frequency

Back 91

1. by the pressure transduction of the bones (1.7x)
2. by the diff in SA of tympanic membrane and oval window (17x)

total = 22x

500-2000Hz

Front 92

muscles that control ossicles

Back 92

tensor tympani - attached to malleus
stapedeus - attached to stapes

they activate reflexively or sounds over 80db or for sounds you make yourself

Front 93

basilar membrane

Back 93

mechanical frequency analyzer (has diff resonant freq. all along its surface due to varying width and eleasticity

Front 94

basilar membrane deflects up vs. down (response in hair cells)

Back 94

excitation vs. inhibition

Front 95

do hair cells fire action potentials?

Back 95

no, release graded responses of glutamate

Front 96

role of calcium in hair cells (3)

Back 96

releases glutamate to synapse when in the base

activating myosin motor molecules to walk up or down actin filaments, creating more or reducing the tension in the tip links

creating electrical resonance through K+ channels (ca activated) in base

Front 97

hair mechanotransduction vs. phototransduction (time scale)

Back 97

microseconds vs. milliseconds

Front 98

tuning characteristics of hair cells (2)

Back 98

hair bundles:
shorter - (higher freq.)
stiffer - (higher freq.)
electrical resonance:
- oscillations of hyper/de-polarizing in the base of hair cells through K+ in and out meovement

Front 99

cochlear amplification (mechanism)

Back 99

Outer ahricells shorten - depolarized
lengthen - hyperpolarized

this moves the basilar membrane up and down more especialy at low amplitude sounds

-makes the tuning curve for each inner hair cell stronger

Front 100

otoacoustic emissions (cause)

Back 100

the movement of outer hair cells causes disturbance of basilar membrane and it comes the other way out (system is reversible)

Front 101

medial olivocochlear neurons

Back 101

efferents that inhibit function of OTC

Front 102

lateral olivochochlear neurons

Back 102

efferent that inhibit ITC

Front 103

afferents response to diff amplitudes

Back 103

sigmoidal
- tapers off at a certain speed (cant fire any faster)
- gets reduced firing response width with different

Front 104

efferent impact on afferent response in inner hair cells

Back 104

- bandwidth of an afferent can be pushed up or down based on efferent inhibition of hair cell
- can help ignore noise (antimask)

Front 105

why are many afferents on 1 IHC not redundant?? (and mechanism)

Back 105

cause they each cover different amplitude ranges

cause of synapse properties and physiological properties of the afferents

Front 106

phase locking

Back 106

preferential firing for a certain phase of a waveform

Front 107

bushy cell (function, where)

Back 107

located in coclear nucleus, keep temporal info about afferent firing that is lost elsewhere for projection to SOC

Front 108

why does cochlear nucleus have 3 copies of tonotopic map?

Back 108

cause it does diff things with each map, and there arent many afferents in aud system

Front 109

interaural sound difference (where, how, for what?)

Back 109

done in medial SOC
- the difference in phase arrivals at each ear for azimuth sounds
- by using a system with delays on contralateral side and ipsilateral all reach at the same time
-neurons are coincidence detectors
- works best for low freq sounds (it phase locks)

Front 110

interaual level difference (where, how, for what?)

Back 110

in lateral soc
- neuron on contralateral side must go through inhibitory synapse
- the total signal sent up depends on if contralateral reaches first (then the signal is weaker as it goes up)
- for hgih freq sounds (amplitude diff is more pronounced)

Front 111

binaural summation columns

Back 111

in A1, crosshatched with sound frequcy excited by either ear's input

Front 112

suppression columns

Back 112

in A1, inhibited by one ear, excited by other ear's input

Front 113

A1 (thigns it codes)

Back 113

freq, binaural columns, and sound location in space

Front 114

environmental noise broadband impact on crit period for sound

Back 114

delays the beggining of it

Front 115

speech processing influenced by touch

Back 115

puffs of air experiment

Front 116

aminoglycosides

Back 116

drugs that are high efficacy, low cost but with side effects that destroy the auditory system

Front 117

hearing loss (patterns)

Back 117

old age,
high frequencies

Front 118

otosclerosis

Back 118

calcification of middle ear bones

Front 119

otitis media

Back 119

ear infections

Front 120

tinnitus (causes)

Back 120

ringing in your ears (can be caused by change in blood flow to your ears or hypersensitivity of hair cells to compensate for lost or damamged cells)

Front 121

hearing aid limitations

Back 121

do not recover lost frequencies

Front 122

cochlear implantation

Back 122

electrodes (13) spiral through cochlea and activate things, go through the round window and around the scala tympani

Front 123

associatiative agnosia (what, where)

Back 123

can reproduce drawings but cant name or identify them
- lesion of posterior parital

Front 124

apperceptive agnosia (what, where)

Back 124

can name things but cant accurately reproduce
- lesion of occipital cortex & areas

Front 125

which areas have neural activity correlating to "knowledge" of an object?

Back 125

- depends on properties of the object (tools show activation in parietal/touch areas)

Front 126

which areas are associated with encoding memory?

Back 126

left Prefrontal association cortex

Front 127

which areas are associated with retreiving memory?

Back 127

right frontal cortex, precuneus

Front 128

stronger pairing of US and CS depends on:

Back 128

continegency not continuity

- reduced presence of the CS without US
- US can be present without the CS and it does not affect learning

Front 129

electroconvulsive therpy disrupts what type of memory?

Back 129

recently consolidated lont term memory (not working memory)

Front 130

non associative learning (2 points)

Back 130

implicit,
- needs 1 stimulus
ex: sensitization

Front 131

associative learning

Back 131

- pairs 2 stim
-operant or classical conditioning

Front 132

experiential response

Back 132

stimulated certain parts of the brain and patients described vivid memories

Front 133

source amnesia (what, where)

Back 133

memories, but dont know from when/why/how

Front 134

4 steps to episodic/semantic knowledge

Back 134

encoding (exposure for the first time from WM)
consolidation (done by proeitn synth and genetic activation)
storage (unlimited in theory)
retrieval ( can change the memory, creative)

Front 135

working memory parts (3)

Back 135

attentional control system (prefrontal)
articulatory loop (words/#s)
visiospatial sketch pad (occipital/parietal areas ie. area LIP)

Front 136

appetitive/defensive conditioning

Back 136

food + CS / pain + CS

Front 137

locations of classical conditioning

Back 137

cerebellum (vermis, interpositus nucleus)
amygdala

Front 138

layer 4C ODCs, nature or nurture?

Back 138

nuture (develop within 13weeks)

Front 139

why do ODCs exist?

Back 139

because of overlap in visual feild for each eye input (3eyed frog experiment)

Front 140

NMDA receptors role in ODC development

Back 140

activation - ODCs develop
blocking - ODCs dont develop

Front 141

LGN eye dominance development (nature/nurture? time course)

Back 141

- eye specific lamnae at birth
on-off sublaminae in some other species

Front 142

Ntrophins: NGF, NT3, BDNF, Nt 4,5 role in ODC development??

-physiology behind this???

Back 142

NGF and NT3 > keep ODCs

BDNF NT2,5 > eliminate ODCs

Those that fire together hit a threshold for Ntrophic release from post synapse and this recruits more axons from same eye
>> its the fact that they fire together (come from the same place)

Front 143

two things that contribute to neural development

Back 143

molecular guidance cues (nature)
maintained neural activity (nurture)

Front 144

threshold

Back 144

50% correct detection of presense of a stimulus

Front 145

what determines relationship between stim. magnitude and perceptual magnitude

Back 145

often can be traced down to the afferent coding

Front 146

how do pac capsule morphology influence their adaptive qualities??

Back 146

many laminae, outer laminae absorb the constant pressure after a while so they are only sensitive to change

Front 147

feedback inhibitory interneurons

Back 147

are often the ones that define smaller receptive areas in somato relay neurons

Front 148

two processes of attn

Back 148

selection, modulation of selected info

Front 149

two ways to calculate d'

Back 149

separation/spread and false alarms -hits

Front 150

presbyopia

Back 150

your lens becomes stiff cant accomodate as well

Front 151

astigmatism

Back 151

shape or lens or cornea is irregular

Front 152

evidence for colour opponent theory

Back 152

- cant see red/green
- stim of same RFs for gang produces opposing responses to diff wavelength
- adapting to one colour makes u more senestive to the ther

Front 153

constructional apraxia

Back 153

posterior parietal lobe damage, cant create spatial relationships in the contralateral visual field

Front 154

delayed response task

Back 154

have to remember which cup the food was underneath (working memory issue, tests lesion of frontal association cortex)

Front 155

why are phtorecpetors at the back of the eye???

Back 155

maybe cause their high demand for blood

Front 156

the solution to limited dynamic range is ______

Back 156

light adaptation

Front 157

explanation for the hermann grid illusion

Back 157

on center geng cell responses are weaker at interesctions cause there is more light in the surround

Front 158

most common colour blindness

Back 158

red-green (deuteranomly)

Front 159

subcortical visual connections (2)

Back 159

retina --> superior collicus (involved in chronometry)
90% of synapses to the LGN are feedback form the visual cortex (might be involved in attn)

Front 160

how is V2 organized??

Back 160

thick, thin, pale stripes

Front 161

magno tract from eye to v5 (5)

Back 161

magno ganglion cells > layers 1 and 2 in LGN > 4c alpha in V1 > 4b in V1 > thick stripe in V2 > V5

Front 162

early directional MT cell response

Back 162

same as V1, perpendicular to the bar's orientation

Front 163

later MT cell response to motion

Back 163

corrects the aperture problem by inhibiting info from non-endstop cells. the endstop cells find the corners and activate those

Front 164

motor units activated later have (2)

Back 164

more force and faster contraction

Front 165

stimulation of the gamma motor neuron ______ the muscle spindle

Back 165

contracts/shortens

Front 166

activation of gamma motor neurons allows the spindle to::

Back 166

reset to a base length proportionate to that of the muscle

Front 167

spinal pathway stength can be modulated at 3 sites:

Back 167

1) pre afferet-interneuron synapse
2) post afferent-interneuron synapse
3) interneuron - motorneuron synapse

Front 168

long latency response

Back 168

must travel up the spinal cord

Front 169

soleus H-reflex

Back 169

vestibular systems involvement in orienting you towards the sun

Front 170

vestibular spinal reflex (purpose)

Back 170

catch yourself when falling

Front 171

vision and movement

Back 171

linear vection and rotation of visual world causes postural changes

Front 172

tocuh and movment

Back 172

helps balance, electronic tactile vest

Front 173

the reafference copy of movements is an _______ input to the sensory afference

Back 173

inhibitory

Front 174

SEF (reference frame)

Back 174

object centered

Front 175

how do head-direction cells build their coding???

Back 175

through vestibular input integration probably

Front 176

medial temporal role in spatial cognition (2)

Back 176

- memory of places (spatial memory)
- place cells in rats

Front 177

the three steps of sensation

Back 177

1) stimulus
2) events to transofrm stim into nerve impulse
3) response (perception)

Front 178

sensory systems convey 4 types of info:

Back 178

1) intensity
2) location
3) modality
4) timing

Front 179

the labelled line code

Back 179

that each sensory system has separate tracts and they dont mix up

Front 180

submodalities

Back 180

receptors with speciifc bandwidths (ie. cones vs. rods)

Front 181

what determines the spatial resolution of a sensory system?? (2)

Back 181

density of receptors, size of RF

Front 182

weber's law

Back 182

delta S (the just notiiceable diff) = k*S (different for each modality)

Front 183

fechner's extension, Steven's mod

Back 183

they both measure intensity of a sensation.

I = k*log(S/So) I = intensity of sensation, So = lowest stimulus strength detectable/ Steven changed this to a power law

Front 184

what encodes intensity of stimulus???

Back 184

firing rate of afferents

Front 185

d' (formula, two ways)

Back 185

separation/spread. or false alarms - hits

Front 186

d' values meanings

Back 186

d' < 1, a lot of overlap (high signal to noise ratio)

d' > 3, not much overlap

Front 187

ROC curves

Back 187

plot hits over false alrms
if d' = 0, its a diagonal line

Front 188

three types of inhibitory interneurons

Back 188

feedforward, feedback, distant inhibition

Front 189

hardware filters on the brain vs. software filters

Back 189

cortical space vs. attention

Front 190

two parts of attention (2)

Back 190

1) filtering - deficit: can lead to autism
2) modulation

Front 191

attention ______ neural responses to behaviourally relevant stimuli in visual neurons

Back 191

enhances

Front 192

why arent ODCs completely nurture???

Back 192

cause they have a critical period for development

Front 193

glutaminergic receptors (2)

Back 193

NMDA, AMPA

Front 194

NDMA receptors and ODCs

Back 194

they help LTP and pruning of ODCs

Front 195

LGN (nature or nurture??)

Back 195

nature, separated at birth already

Front 196

neurotrophins (which ones help ODC development?)

Back 196

NGF or NT3. NT4,5,BDNF do NOT cread ODCs

Front 197

orientation, nature or nurture??

Back 197

nature, bu degenerate if not used

Front 198

imprintation (birds)

Back 198

birds become imprinted to any moving object in their environment after birth

Front 199

hospitalism

Back 199

develops when kids dont get enough parental care before a certain age

Front 200

experiential response

Back 200

vivid memories as if experiencing them from brain stimulation

Front 201

amygdala's role in explicit memory

Back 201

none

Front 202

left vs. rigth hippocampus (type of memory)

Back 202

left: words, people, objects. right: spatial memory

Front 203

source amnesia (how it happens, what)

Back 203

lesions of frontal lobe. remember an event but now how or when it happened

Front 204

WM neurons memory selectivity

Back 204

- can be selective for sifferent qualities (ie. different values of numbers)

Front 205

DA d1, d2, d3 receptors and WM

Back 205

bad for memory = d1. antagonists improve WM. good for memory = d2,d3. antagonists suppress WM

Front 206

LIP and working memory

Back 206

Lateral intraparietal cortex neurons also show delayed activity during working memory tasks

Front 207

DLPFC and working memory

Back 207

impt for attention. if DLPFC is lesioned, cant memorize im presence of distractors

Front 208

working memory conceptualized as

Back 208

articulatory loop, visiospatial sketchpad, episodic buffer

Front 209

cerebellum and classical conditioning

Back 209

vermis and nucleus interpositus play a role.

Front 210

what pick pockets use to get you

Back 210

habituation and sensitization

Front 211

electroconvulsive therapy and memory

Back 211

disrupts memories recently committed to long term

Front 212

reinforcer

Back 212

a good reward given to an animal after a certain behaviour (food) THAT CAUSES IT TO LEARN

Front 213

law of effect

Back 213

that +vely reinforced behaviours happen more often and negatively reinforced behaviours are not repeated

Front 214

anatomical organization of ANS pathways (general)

Back 214

CNS > preganglionic fiber >autonomic ganglion > postganglionic axon

Front 215

3 divions of ANS

Back 215

sympa (fight), para (rest)) and enteric (digestive/internal organs)

Front 216

sympathetic divison of ANS

Back 216

- dialates the eyes, speeds the heart, lungs faster, digestive slows down
- ganglia close to spinal cord

- adrenal medula is an effector organ (when activated, produces ADR and NORADR)

Front 217

peristaltus

Back 217

- incrase or decrease of activity in the intestines

Front 218

vagus nerve and ANS

Back 218

vagus nerve caries a lot of the parasympathic axons

Front 219

sensory info and ANS integration (where)

Back 219

at the NST which projects to medulla/spinal cord
b) lateral medullary RF for autoreflexes ie. vomiting

Front 220

fakir

Back 220

people in India who can control heart rate and autonomic reflexes

Front 221

sympathetic NTs

Back 221

ACh (pre gang), NE (post gang)

Front 222

parasympathetic NTs

Back 222

ACh (pregang), ACh(post gang)

Front 223

ACh receptors (3)

Back 223

nicotinic fast PSPs, muscarinic: slower PSPs, peptidegic: releases neuromodulators

Front 224

hypothalamus influences 3 systems to achieve homeostasis

Back 224

ANS, motivational system, endocrine system

Front 225

parasympathetic preganglion cell (location)

Back 225

most preganglion cells are from brainstem, the preganglion cells for the sacral parts of the body are located on the sacral spinal cord

Front 226

myenteric plexus, submucous plexus

Back 226

in the enteric nervous system. responsible for gut motility and secretion respectively

Front 227

NST (inputs3, inputs locations 4)

Back 227

inputs: cranial nerves 7,8,9. taste, gastrointestinal, cardiovascular and then resp (from anterior to caudal)

Front 228

NST (projections 3)

Back 228

1) preganglionic neurons in medulla & spinal cord
2) Lateral medullary reticular formation (patterned autonomic reflexes, vomiting)
3) CNS networks (pons > hypthalamus > amygdala, cerebral cortex

Front 229

autonomic reflexes (5 classes, OCGGU)

Back 229

Ocular reflexes (control of pupils’ diameter and
focusing the lens)
• Cardiovascular Reflexes (Blood pressure, heart
rate, baroreceptor reflex, carotid sinus massage)
• Glandular Reflexes (nasal, lacrimal,
gastrointestinal)
• Gastrointestinal Reflexes (control of gastric acid
secretion (S and PS), Peristalsis (enteric system))
• Urogenital reflexes (Bladder emptying, sexual
reflexes)

Front 230

adrenal medula NTs

Back 230

thoracic gang (ACh) > adrenal medulla (E and NE)

Front 231

compounds (pharmacology) that impact ANS (3 examples)

Back 231

STIMULANT atenolol (used to reduce hypertension, adrenergic beta 2 antagonist),

RELAXANT salbutamol (bronchiod, asthma reduction, adrenergic beta agonist),

atropine (fox gloves flowers, antagonist of muscrinic ACh receptors (reduced drooling in Parkinsons)

Front 232

NPY, somatosin, enkephalins* are examples of

Back 232

noradrenergic (NE) neurotransmitters. Enkephalins are INHIBITORY

Front 233

vasoactive intestinal polypeptide, calcitonin gene-related peptide, substance b, neurotensin

Back 233

examples of cholinergic (ACh) neurotransmitters

Front 234

coordination of autonomic nervous functions NPPAV (5 areas)

Back 234

Nucleus of the Solitary Tract (stomach, heart
rate, blood flow)
• Parabrachial nucleus (gustatory processing)
• Periaqueductal gray matter (fight-or-flight)
• Amygdaloid Complex (autonomic component of
conditioned behavior)
• Visceral sensory areas of Thalamus (VPPN) and
sensory cortex (insular cortex, infralimbic area)

Front 235

the general role of the hypothalamus

Back 235

Integrates autonomic responses
with behavior

Front 236

5 things the hypothalamus controls/regulates (BTMRS)

Back 236

- bp & electrolytes
- tempurature
- energy metabolism
- reproduction
- emergency response to stress

Front 237

hypothalamic mechanims (3 steps)

Back 237

1) receives sensory info from entire body
2) compares with biological set points
3) responses to restore homeostasis (autonomic, endocrine or behavioural)

Front 238

hypothalamic divisons (3 areas, their functions)

Back 238

Anterior or pre-optic area: integration of sensory
information for comparison with set point.
Controls blood pressure and composition,
circadian rhythm, reproduction, hormones.
• Middle area: endocrine and autonomic functions.
Controls the pituitary gland, growth, feeding,
maturation and reproduction.
• Posterior area: mammillary body (???).
Tuberomammillary nucleus that regulates
wakefulness and arousal.

Front 239

Two types of hypothalmic endocrine control, an example of each

Back 239

direct: Magnocellular neuroendocrine neurons
in nuclei paraventricular and supraoptic
secrete oxytocin and vasopressin (milk
release and water balance).
indirect • Parvocellular neurons secrete releasing
factors that control pituitary secretions.

Front 240

The paraventricular nucleus of the hypothalamus

Back 240

is a microcosm of the autonomic and endocrine control systems

Front 241

emotion (structures, two types of arousal)

Back 241

a bodily state.
- stimulus filtering and evaluation done by cortex and subcortical structures. then they impact the skeletomotor and autonomic control systems
- general arousal, specific arousal

Front 242

feeling (structures (3))

Back 242

a conscious sensation.
- cerebral cortex, cingulate, and frontal lobe

Front 243

james-lange theory

Back 243

- feelings occur after info about physiological state
- evidence:spinal cord lesions, reduction in emotions
- criticisms: emotions outlast physiological changes and symp response is undifferentiated

Front 244

canon-bard theory

Back 244

-hypothalamus and thalamus regulate peripheral emotion
- cortex: cognitive processing of emotion

proof: sham rage in cats

Front 245

Schachter-Damasio theory

Back 245

• The cortex actively translates peripheral signals
into cognitive response.
• It creates a cognitive response to peripheral
information consistent with the individual
expectations and social context (epinephrine
injections).
• Damasio: Emotions are stories that the brain
creates in order to explain bodily reactions.

Front 246

arnold's theory

Back 246

emotions: unconscious evaluation of a situation (implicit memory). proof: emotional reaction to subliminal stimuli.
feelings: conscious & determine tendency of response (explicit memory)
peripheral component: hypothalamus
central component`: cerebral cortex, cingulate and prefrontal
amygdala: coordinates conscious experience and peripheral expressions (fear)

Front 247

hypothalamus role in emotion and lesions (2)

Back 247

-peripheral expression
- lesions of lateral HPT: placid
- lesions of medial HPT: aggressive

Front 248

papez circuit extended by mclean

Back 248

cingulate > hppcmpus > mam. body > anterior thalamic nuclei > cingulate

Front 249

the limbic system

Back 249

cortical areas involved in emotion/feeling

Front 250

kluver brucy syndrome (how, symptoms)

Back 250

**removal of the amygdala and hppcampal formation
– flattened emotions
– increase in sexual behavior
– compulsive tendency to observe and react to every visual
stimulus but failure to recognize familiar objects

Front 251

urbach-wiethe disease (how, symptoms)

Back 251

(calcification of the
amygdala), disrupts the unconscious processing of
cues to fear

Front 252

classical fear conditioning and the amygdala

Back 252

- amygdala lights up for fearful stim, not for happy stim, maybe cause fear requires more immediate responses
- lesions of the amygdala abolish this

Front 253

basolateral nucleus of the amygdala, central nucleus of the amygala, nucleus basalis of the amygdala (functions)

Back 253

1) receives sensory info from thal
2) impacts the AEB systems
3) sends the info the the cortex

Front 254

removing frontal cortex and emotion

Back 254

calming effect on chimpanzees

Front 255

vental frontal lobe lesions and emotion

Back 255

disinhibition of inappropriate behaviour

Front 256

hippocampus and emotions

Back 256

indirect role

Front 257

motivational states (2 types)

Back 257

elementary drive states: hunger, thist, temperature.
personal or social aspirations

Front 258

servomechanims

Back 258

• Maintain a controlled variable within a certain range
• Feedback detector that compares a measure value
with a set point
• Integrator generates an error signal when the value of
the controlled variable does not match the set point.
This signal is use to drive controlling elements

Front 259

temperature regulation

Back 259

- integrator is in the hypothalamus
- posterior HYP: heat conservation
- anterior HYP: heat dissapation
- warm and cold sensitive neurons in preoptic area
-antipyretic (against fever) area: septal nuclei near anterior commisure

Front 260

feeding behaviour set points (why it changes, lesions)

Back 260

- body weight is a set point that can vary
-with stress,
palatability of the food, exercise, and
environmental and genetic factors

ventromedial nucleus lesion: raises the set point
lateral hypothalamus lesion: lowers the set point
*** but these are NOT feeding/satiety centeres, just control further down processes
***they change the set point, not the feeding behaviour

Front 261

Cues that control food intake (short term, long term, horomones)

Back 261

short term: blood glucose, intestinal hormones
long term: leptin from ob gene (inhibits release of NPY in hypothalamus, stopping feeding behaviour)

Front 262

double depletion hypothesis

Back 262

for drinking behaviour, that its controlled by:
*tissue osmolarity (amount of water in tissue) - sensed by osmoreceptors in hypothalamus
*vascular volume (amount of blood) - right atrium, great veins, and carotid sinus. kidneys release renine in response to low vascular volume

Front 263

other factors that regulate motivational states (3)

Back 263

• Ecological requirements of the
organisms (specific vitamins or cholestrols needed)
• Anticipatory mechanisms (circadian
rhythm)
• Hedonic factors (pleasure)

Front 264

NT effects of cocaine and amphetamine

Back 264

increase dopamine in N. accumbens (block dopamine transporter)

Front 265

NT effects of nicotine

Back 265

enhance DA release by action on presynaptic cholinergic receptors

Front 266

mew opiod agonists

Back 266

increase DA in VTA by inhibiting GABA-neurons that suppress DA

Front 267

dopaminergic pathways

Back 267

mesolimbic (motivation) (NA and VTA)
nigrostriatal (movement) (BG and SN)
ventral tegmental

Front 268

cocaine and nicotine effects on self stimulation

Back 268

reduce the frequency of it, because you are already getting enough reward from the drugs.

so: drugs are a lay way to release DA

Front 269

N. accumbens (parts and function in addiction)

Back 269

core and shell. shell is involved in addiction through connections to hypothal and limbic system

Front 270

tolerance, dependence

Back 270

- need more drug to get a high
- negative consequences of withdrawal, can happen even without DA addiction

Front 271

reward circuit (in the rat) (and drugs that act on each part)

Back 271

VTA --------------DA------------> N. Accumbens

drugs on VTA:
cocaine, THC, ketamine, amphetamines, opiates

Front 272

craving also happens through environmental cues

Back 272

cocaine craving example, activation of pathways happens throguh the pictures alone

Front 273

sham rage in cats

Back 273

aggressive response to even light touch, decorticated

Front 274

nativism (chomsky)

Back 274

- there is innate neural circuitry for language

Front 275

empiricism (Skinner)

Back 275

that language is completely acquired through trial and error

Front 276

elements of language (3 variables)

Back 276

-morphology (how its written)
- syntax (the order of it)
- phonology (prosody: the emotion conveyed by the intonation)

Front 277

lanugage dev. in children (4 stages)

Back 277

5-7 months (sounds)
7-8 months (syllables)
1 year (sentence like streams)
2 years rich phrase structures

**slower if learning 2 languages

Front 278

Williams syndrome

Back 278

normal language, mental retardation.

Front 279

fasciculus that connects brocas and wernike's areas

Back 279

arcuate fasciculus

Front 280

the three systems for language processing:

Back 280

- language implementation (Broca’s and Wernicke’s areas, insular cortex,
basal ganglia) analyze incoming signals so as to activate conceptual
knowledge, grammar and articulation.
- mediational system (regions of frontal, temporal and parietal association
cortices)
- conceptual system (collection of regions in the higher order association
cortices, supports conceptual knowledge)

Front 281

broca's aphasia

Back 281

speech and articulation impaired. broca's area might be related to short term memory for language. depressed. cant repeat.

Front 282

wernike's aphasia

Back 282

speech doesnt make sense, fluent. might process speech sounds/associate them with concepts. anxious/paranoid. cant repeat.

Front 283

conduction aphasia

Back 283

dmg to STG and IPL, cant repeat. can speak and understand pretty normally well

Front 284

transcortical motor aphasia:

Back 284

damage to left DLFA and left SMA. cannot initiate spontaneous speech. cant repeat.

Front 285

Transcortical sensory Aphasia

Back 285

fluent speech, impaired comprehension and some trouble naming things, knowing meanings

Front 286

global aphasia

Back 286

combination of broca, wernike and conduction aphasias

Front 287

other brain areas impt for lanuage (3)

Back 287

1)left temporal cortex (words pertaining to categories)
2)insula (planning and coordinating articulation)
3) SMA and cingulate cortex (initiation and maintenence of speech)

Front 288

right hemisphere in lanuage

Back 288

emotional prosody, pragmatics of language (narratives, jokes, etc). can take over lang function before a critical period

Front 289

scopolamine (what it is, role in WM)

Back 289

muscarinic ACh receptor antagonist. causes reduced working memory in PFC

Front 290

hippocampus anatomy

Back 290

entorhinal cortex --------perforant pathway--------> dendate gyrus granule cells-----mossy fiber pathway-----> CA3 pyramidal -----schaffer's collateral----> CA1 pyramidal------> subiculum

Front 291

do london taxi drivers have larger hippocampus??

Back 291

no, but posterior is larger and anterior is smaller than avg person

Front 292

continual neurogenesis

Back 292

in hippocampus, underlies formation of new memories

Front 293

3 things needed for spatial navigation

Back 293

1) internal compass
2) external landmarks
3) neural representation of environment

Front 294

function of CA3 in spatial memory

Back 294

accuracy of memory of places in space

Front 295

tetrode

Back 295

used to record multiunit neural activity (put in rat brain)

Front 296

CA1 sppatial place fields (2)

Back 296

firing of pyramidal cells here is:
1) encoding location
2) NO diretional selectivity (omnidirectionality)
3) stable over time (impt for memory)
4) has no topographic organization

Front 297

spatial working memory

Back 297

happens through path integration
- pattern of place cells that fire when taking a specific path

Front 298

distributed representation (in spatial position coding)

Back 298

the pattern of CA1 cells that fires is different for each position

Front 299

remapping of place fields (when it happens (3), when it doesnt happen (5))

Back 299

remapping of place fields happens when landmark positions are
YES
1)landmarks rotated without the animal's knowledge
2) addition of novel landmarks in the activated place field without knowledge (random remap)
3) removal of landmarks without knowledge (random remapping)

NO
1)landmarks rotated with animal's knowledge
2) landmarks translated
3) landmark shape changes
4) landmark environment changes size (to scale)
5) landmark removal outside of place field

Front 300

in case of external and self-motion cue contradiction, which dominates???

Back 300

self-motion cues

Front 301

in case of dital and proxmial landmark rotation contradiction, which dominates???

Back 301

both have influence

Front 302

experience dependent changes in place fields

Back 302

running a stereotyped route activated place cells in a specific order and streched the activation pattern

Front 303

place cells in humans vs. rats

Back 303

humans have less, only cover most of the environment, also might be 3D compared to rats 2D

Front 304

synpatic knob membrane

Back 304

the part of the membrane where the veiscle merges with the synpase surface

Front 305

Hebb's postulate:

Back 305

cell A ------<| cell B

* the connection gets stronger each time they fire together. this is what underlies plasticity

Front 306

tetanus

Back 306

periodic pulse train of stimulation

Front 307

1Hz vs. 10Hz stim of schaffer collateral pathway

Back 307

induces LTD vs. LTP

Front 308

NMDA glutamate receptors (mechanism)

Back 308

- only activated when membrane depolarizes (MG++ block comes out)
- permeable to calcium

Front 309

APV and EGTA (effects, at hgih and low concentration, mechanims)

Back 309

molecules that stop potentiation
1) APV stops things from entering NMDA receptors (low concentration, makes LTP into LTD. high concentration, no plasticilty possible)
2) EGTA prevents calcium from interacting with things in the cell ([low] = LTP. [medium] = LTD. [high] = no plasticity)

Front 310

LTD (mechanism)

Back 310

Ca enters, starts dephosphorylation (phosphatases) signalling cascade pulls AMPA receptors out of membrane. more efficiently activated by low levels of Ca.

Front 311

LTP (mechanism)

Back 311

Ca enters, starts phosphorylation (kinase) signalling cascade puts AMPA receptors into membrane. more efficiently activated by high levels of Ca.

Front 312

plasticity and place fields

Back 312

plasticity needed for retention of stable place fields.

Front 313

spike timing dependent plasticity (mechanism, what it does)

Back 313

cell A (excitatory)----<| cell B

(within 40ms)
if you make cell A fire before B, it will increase cxn
If you make B fire before A, it will decrease cxn

**predicts shifting of place fields (cause you activate neurons in a sequential order in time), ONLY if movement is stereotyped. thats why place fields are stable. cause we always move different directions

Front 314

STDP can be anti-hebbian (where?)

Back 314

cerebellum

Front 315

children learning anguage vs. adults learning laguage

Back 315

watch lips vs. watch eyes

Front 316

habituation/dishabituation (as a response, neural mechanism)

Back 316

to harmless stimuli (release of less NT)/to harmful stimuli (axoaxnoic serotinergic cxn on pre-synapse terminal increases NT release)

Front 317

short vs. long term habituation (neural mechanims)

Back 317

less vesicles docked and released vs. fewer synaptic connections

Front 318

short vs. long term habituation (neural mechanisms)

Back 318

less than 4 shocks (5HT binds g protein, PKA allows more Ca in, K out, and docks vesicles). vs. more than 4 shocks (ubiquitin hydrolase is transcribed, makes PKA do its job all the time)

Front 319

protien kinase A actions in short term facilitation (2)

Back 319

1) catalytic subunits (close K channels, open Ca channels)
2) regulatory subunits (dock more vesicles)

Front 320

characteristics of language development (5)

Back 320

1) spontaeous
2) exposure to vocalizations early is critical for vocal learning
3) practice leads to a match between model and imitation
4) loss of feedback causes a gradual deterioration
5) social interactions influence dev. of vocal learning

Front 321

spectograph

Back 321

used to represent the highly structured nature of human speech

Front 322

how do male wcs and zebra finches learn their song??

Back 322

through a tutor (father)

Front 323

song learning stages (3)

Back 323

listening (day 30-70), practice (35-90), crytalization (90)

Front 324

song learning is creative

Back 324

if they have two tutors, will make a song that is a composite of the two. it also depends on the place

Front 325

error-driven model for learning and maintaining song

Back 325

1. storage of a template
2. song production
3. song feedback (acoustic and motor)

Front 326

lesions in bird brain area X (juveniles vs. adults)

Back 326

disrupts song learning vs. has no effect

Front 327

for the bird to learn ABCDE (sequential learning)

Back 327

bird was presented with D-E, C-D, B-C, A-B. once learned, the bird can do it backwards

Front 328

song in bird brain (anatomy, neuromechanisms)

Back 328

HVC has aud input
- RA projects to syrinx (vocal output)

HVC > RA > Syrinx

:::happens by neural plasticity (blocked by APV and BAPTA)

Front 329

efference copy and reafference stimulus (sensation) combine to give rise to __________. how???

Back 329

perceived stimulus.

the prediction of efference copy is compared with the reafference stimulus, they combine and if theres a difference, then there is a tickle

Front 330

timing of predictive movements (brain area, test)

Back 330

cerebellum, eyeblink conditioning (puff of air with loudspeaker). this doesnt happen with cerebellum lesion.

Front 331

cerebellum anatomy

Back 331

- 4 layers
-granule cells ----parallel fibres---<| purkinje cells ------climbing fibers---<|

Front 332

motor learning (recalculation and motor adaptation)

Back 332

- throwing the putty experiment. cerebllar damage doesnt allow for recalculation
- adaptation is error driven

Front 333

electric fish

Back 333

- highly developed cerebellum
- needs it to keep up with the change in electrolocation as it grows

Front 334

electric organ discharge command

Back 334

- if altered by a stimulus (inhibitory/excitatory)
- it does a bounce back when you take that stimulus away (anti-correlation)

Front 335

electric fish: changes in the reafferent stimulus cause changes in the efference copy (mechanism)

Back 335

mechanism is anti-hebbian STDP! (cancellation of reafferent input)

Front 336

PTSD and long term learning

Back 336

linked by CREB (translator protein for ubiqutin hydrolase and those other things that cause LTP)

Front 337

barnes maze test

Back 337

rat has to find the correct hole

Front 338

direction of secondary (extraceullar) vs. primary (intracellular) currents

Back 338

they are opposite directions

Front 339

MUA vs. LFP frequencies

Back 339

> 400hz = MUA. lower than 150Hz = LFP

Front 340

deoxyHb vs. BOLD

Back 340

down, up

Front 341

dip, rise, dip in BOLD signal - explain:

Back 341

oxygen consumption, CBF overcompensation, CBV increase

Front 342

intrinsic signals

Back 342

- image deoxyHb/oxyHb by their absoption spectra. at a wavelength of 605nm, the differences are large

Front 343

voltage sensitive dyes

Back 343

emit light based on membrane potential threshold difference

Front 344

oxygen metabolism and spiking activity

Back 344

shown to be correlated by optical imaging

Front 345

is there ever a non-linearity with BOLD ~ LFP/MUA activity???

Back 345

yes, in the cerebellum climbing fiber stimulation

Front 346

signal to noise ratio: more neural or hemodynamic??? consequences?

Back 346

more in hemodynamic. this means the actually neural activity is underestimated by a lot

Front 347

fluctuations in resting state networks

Back 347

slowwww

Front 348

DMN anticorrelated with

Back 348

dorsal attention network

Front 349

hypothesis on the role of default mode network (4)

Back 349

- self referential processes
-introspection
-ongoing consciousness and awareness
-there is altered DMN activity in sleep and psychopathologies like schitz, depression, mild cog impairments and alzheimers

Front 350

non-neurophysiological confounds to fMRI signals

Back 350

1) respiration induced signal changes

Front 351

3 scales to neurophysiology

Back 351

micro: cells
meso: micro-columns and their connections (sideways)
macro: anatomically segregated

Front 352

how to image at the meso scale???

Back 352

- voltage sensitive dyes

Front 353

spontaneously occuring state vs. evoked state

Back 353

70% amplitude vs. 100% amplitude

Front 354

resting state at meso scale

Back 354

shows higher probability than chance of functional correlation with active networks

Front 355

What can spontaneous activity and restingstate
networks be used for? (3)

Back 355

- Analyzing the pattern of connections between areas in
the healthy human brain
- Potentially, for diagnosing neurological and psychiatric
conditions
- Potentially, for serving as bio-markers for progression of diseases

Front 356

What is the functional role of spontaneous
activity and resting-state networks? (4)

Back 356

- NOTHING: An essential property of the neural architecture
underlying cognition.
- INFO PROCESSING: involvement in functionally relevant information
processing.
- ACTION: a non-random, coordinated interaction of ongoing and
evoked activity in perception and behavior.
- VIGILANCE: scanning of context possibilities, making it easier to
lock on a concurrent ‘scene’ or stimulus.

Front 357

scale from largest to smallest: circuits, systems, maps, neurons

Back 357

(10 cm)systems, maps, circuits, neurons (.1mm)

Front 358

population activity vs. single neuron activity

Back 358

population activity reflects the activity of single neurons very well

Front 359

differences in hand and eye control (5)

Back 359

1) limbs have more joints than the eye
2) geometry of limb muscles is complex
3) eye does not have strech reflexes
4) eye does not carry loads
5) limb movements require adjustment in posture

Front 360

kinematics vs. dynamics

Back 360

Movement of hand (and joints)
through space vs. forces required to elicit observed
kinematics.

Front 361

how do you know M1 neurons go down corticospinal tracts??

Back 361

short latency responses using EMG

Front 362

M1 is not simple output station (2):

Back 362

- a single neuron can stim many muscles
- many neurons stim the same muscles (redundancy allows different approaches to muscle movement ie. power grip vs. prescision grip)

Front 363

activity of M1 vs. muscle EMG

Back 363

- not perfectly correlated

Front 364

what do M1neurons encode??

Back 364

1. firing rate varies with amount of force
2. direction of the mvement (broadly tuned)

Front 365

spike triggered averaging

Back 365

- average all the spikes in EMG activity, find the latency and use that to determine if the neural activity caused the muscle movement

Front 366

do M1 neurons encode dynamics?

Back 366

yes, cause they activate the muscle (evidence: STA)

Front 367

preferred direction

Back 367

direction of movement that maximally activates a nuron

Front 368

population vector

Back 368

the sum of all the resultant vectors for PD in m1 neurons. it is a good approx of the direction of motion

Front 369

applying a force to the opposite of the preffered direction of a neuron will do what???

Back 369

increase the firing rate of the cell

Front 370

proprioceptive feedback involves information from (the future, present, or past)

Back 370

past

Front 371

what consequence does delayed feedback have on output??

Back 371

- creates oscillations in output that can become uncontrollable

Front 372

internal model (what, purpose)

Back 372

predicts the sensory consequences of a motor command drawing on past experience

purpose: compensates for delay, predict consequences, allows the brain to choose a movment optimized for relevant variables

Front 373

real effects of imagining neuron commands

Back 373

1) if executing a difficult movement takes a long time, then imagining that movement also takes a long time
2) autonomic function increases during imagined movement

Front 374

main function of forward models

Back 374

to ensure correct operation of feedback systems

Front 375

plant

Back 375

system to be controlled (eye, hand, etc.)

Front 376

to compensate for delays

Back 376

use a forward/internal model

Front 377

evidence of predictive control in the saccadic system

Back 377

when your eyes are tired, they still land at the same spot from a saccade as earlier in the day. how?? your brain knows to correct based on the internal model for tired saccades

Front 378

feedback systems use _______ to estimate feedback signals

Back 378

forward models

Front 379

LIP neurons vs. MIP neurons

Back 379

predictive eye movements vs. predictive hand movements

*both project to areas in the frontal cortex involved in hand eye coordination
*both have eye centered reference frames

Front 380

signals that best correlate with past, current, and future movments

Back 380

feedback, the prediction, and efference copy

Front 381

areas in the brain that are part of a forward model of movement

Back 381

PPC, cerebellum, dorsal premotor cortex

Front 382

voluntary movements (3)

Back 382

1) have a purpose (not reflexive)
2) are guided by some reward or perveived gain
3) can be learned and improved

Front 383

people follow vision more than proprioception until what point??

Back 383

more than 10 degrees of proprioceptive turn

Front 384

models for hand centered targeting (2)

Back 384

1. direct transformation: eye centered target + eye centered hand = hand centered target

2. gradual: eye centered target + eye in head position = head centered. head centered + head on body position = body centered. body centered + body-centered-hand = hand centered target.

***there is evidence for both!

Front 385

the same point can be described by many reference frames (examples)

Back 385

cartesian coordinates and polar coordinates. need to be transformed from one to another, just like movement reference frames!

Front 386

memory (delay) reach task functions (4)

Back 386

1) separates sensory from motor activity in the neuron activated by the task
2) causes neurons inMIP to increase firing rates
3) forces subject to remember location of the target
4) forces subject to control when to to reach

Front 387

reference frame task

Back 387

you use the reference frame that keeps things constant the most

Front 388

reference frame for neurons in area 5

Back 388

encode the target in a reference intermediate beetween the hand and eye.

***allows for target encoding relative to hand AND eye
can be correlated with various ones: hand, body, eye centered as well (weaker correlation)

Front 389

gain fields

Back 389

a nonlinear way to combine inputs
*one input modulates the sensitivity of a neuron to another input (multiplication)
* can be used to compute coordinate transformations
- therefore: gradual model is just as likely as direct model for reaching