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PSYC211 > Jones > Flashcards

Jones Flashcards

1
Q

how long does it take u 2 make choice n execute command when choosing between 2 things

A

350-450ms

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2
Q

what makes up the CNS vs. peripheral nervous system (broad)

A

CNS = brain + spinal cord; peripheral nervous system (PNS) = everything else

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3
Q

what can the PNS b divided in2

A
  1. somatic nervous system - part of nervous system interacting w/ external enviro →
    afferent n efferent nerves
  2. autonomic nervous system (regulating body’s internal enviro)
    →
    afferent n efferent nerves (efferent nerves here further divide into parasympathetic n sympathetic nervous systems)
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4
Q

afferent vs. efferent nerves

A

afferent = input/info going in; efferent = output

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5
Q

parasympathetic vs. sympathetic nervous system

A
  1. parasympathetic: relaxation (‘rest + digest’)
  2. sympathetic: involved in physiological arousal (‘fight or flight’)
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6
Q

describe the 12 cranial nerves connected directly 2 brain

A
  1. each cranial nerve sends signals 2 brain (e..g. info that’s been computed thru sense organs)
  2. all cranial nerves part of PNS, save cranial nerve #2 (optic nerve) which is part of CNS
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7
Q

name (+ loosely describe) the 31 pairs of spinal nerves which r connected via spinal cord

A
  1. nerves exit or come in frm above or below vertebrae
  2. cervical nerves = nerves C1-C8
  3. thoracic nerves = T1-T12
  4. lumbar nerves = L1-L5
  5. sacral nerves = S1-S5
  6. coccygeal nerves (right @ spine base)
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8
Q

how do u get the sensory dermatome (covers entirety of body) frm nerves?

A

each nerve encodes a diff part of the body

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9
Q

does the dorsal or ventral part of spine receive sensory input

A

dorsal (which is on back of spine btw)

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10
Q

motor neuron that executes command (output) is situated on which side of spine

A

ventral side (front of spine)

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11
Q

2 most significant portions of forebrain?

A
  1. telencephalon - bulk of outer portion of brain (w folds), most interested in outermost layer (avg. 2.5mm thick)
  2. diencephalon - has thalamus !
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12
Q

describe telencephalon in Greater detail - what stains can u use 2 look @ it, what do they show/find

A
  1. contains 6 layers of neocortex, stain brain cells 2 look @ them
    –>
    use Nissl stain (only stains cell bodies) 2 look @ organisation of cortex cells - how r they packed
  2. Golgi stain (only taken up by some cells, but spreads) - shows wiring of cortex/how cells connect 2 each other)
  3. find: cortex arranged into 6 distinct layers based on cell numbers, arrangement, n connectivity
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13
Q

midbrain ?

A

connects forebrain + hindbrain

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14
Q

what’s in the hindbrain

A
  1. metencephalon
  2. myelencephalon
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15
Q

what’s the main site of input in a neuron

A

dendrites duh…

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16
Q

describe axon hillock .

A

cone-shaped place in junction between soma + axon in neuron

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17
Q

nodes of Ranvier?

A

situated in gaps between myelin in neuron

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18
Q

what r ‘buttons’ in a neuron

A

endings of axon branches which release chemicals in2 synapses

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19
Q

what is a neuron’s membrane potential

A
  1. separation of charge between inside + outside of cells
  2. inside of cell kept negative (has approx. -70mV difference compare 2 outside)
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20
Q

what r ions

A

charged particles w either extra or missing electrons in outer shell

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21
Q

cell membrane structure

A

channel protein, signal protein, lipid bilayer

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22
Q

what creates resting difference in charge between inside + outside of neuron - v broad view

A

have pumps in cells membrane which set up situation where more sodium is outside (Na+; positively charged)

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23
Q

how many extra electrons does Na+ have

A

single extra

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24
Q

is potassium (K+) negative or positive

A

it litch says positive…..

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25
Q

how many electrons is chloride (Cl-) missing

A

one

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26
Q

what r channels in the neuron context

A

protein complexes that bridge inside n outside of cells
→ establishment of certain gradients

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27
Q

what’s the concentration gradient like 4 neurons (resting)

A

concentration highest 4 Na+ outside of cell (wants 2 drift n equilibrate)

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28
Q

what’s the electrical gradient looking like 4 neurons

A

positive valence (frm outside neuron) attracted 2 inside of cell (negativity)

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29
Q

how is info transmitted w/in a neuron

A

by transient alterations in the membrane potential produced when ions r allowed 2 cross membrane

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30
Q

when ur looking @ graded potentials, where r u measuring membrane potential frm in the neuron

A

in dendrite

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31
Q

what r EPSPs

A
  1. graded potentials generated @ synapses r EPSPs (excitatory postsynaptic potentials)
  2. they depolarise cell (make inside more positive, more likely 2 fire action potential)
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32
Q

when ur looking @ APs, where in neuron r u measuring membrane potential frm

A

axon !

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33
Q

what threshold of intensity is sufficient 2 induce an AP

A

axon doesn’t respond 2 input until it reaches threshold of intensity (-55mV)

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33
Q

describe summation !

A

if enough EPSPs arrive @ trigger zone b4 they fade, they can build on each other 2 trigger AP (lasting abt 1ms)

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34
Q

describe the voltage-gated sodium channel

A

as cell becomes lil bit depolarised, these channels open allowing more sodium 2 come in
–>
as sodium flows in2 channel, it depolarises local membrane enough 2 open neighbouring sodium channel (gives u massive overshoot during AP)

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35
Q

Describe the Hodgin-Huxley cycle

A

synaptic potential or receptor potential
→ depolarisation of membrane
→ opening of voltage-gated sodium channels
→ sodium going in2 cell
→ further depolarisation etc.

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36
Q

how long do voltage-gated sodium channels stay open

A

1/2 a ms

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37
Q

when do sodium channels close..

A

once u get 2 abt +50mV

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38
Q

how does Hodgkin-Huxley cycle end

A

Na+ (sodium) channels open
→ K+ (potassium) channels open (rising phase)
→ Na+ channels close
→ K+ channels start 2 close (repolarisation)
→ hyperpolarisation

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39
Q

define hyperpolarisation (simple)

A

membrane potential become more negative <3

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40
Q

define repolarisation

A

K+ leaving cell en masse 2 regain negative charge b4 rebalancing

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41
Q

Na+ K+-ATPase pump - what does it do

A

maintains the gradient of a higher concentration of Na+ extracellularly + higher level of K+ intracellularly

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42
Q

how do APs move along axon (ignoring myelination) + what r the issues w that

A
  1. AP moves along axon thru depolarising enough 2 get each Na+ channel 2 open + then moving on2 next one
  2. BUT … AP velocity solely thru opening + closing of Na+ channels is only 0.5-2 metres per second (wayy too slow)
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43
Q

ok so how does myelination help w AP conduction velocity

A

if nodes get more Na+ channels being opened, then myelin conducts that potential faster 2 the next node (opens more Na+ channels)
–>
conduction velocity of up 2 100+ metres per second !!

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44
Q

myelin sheath def (simple)

A

mix of fat n protein (insulation like on a wire)

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45
Q

multiple sclerosis is a result of demyelination (when myelin sheath is lost or starts 2 degenerate)… what r the symptoms?

A
  1. slow, staggered movement
  2. impacts on cognition, vision
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46
Q

how long for neural impulse 2 travel frm toe to spine + back

A

~20 ms

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47
Q

photopic vision. go

A

cones have this, gives them high acuity colour vision in good lighting

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48
Q

scotopic vision. go

A

rods have this, it’s poorer acuity achromatic vision in low-light levels

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49
Q

why do cones have high visual acuity

A

bc they have low convergence - single cone signals 2 single bipolar cell 2 single retinal ganglion cell

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50
Q

why do rods have low visual acuity

A

lots of convergence, pathway goes:
lots of rods
→ less bipolar cells
→ 1 retinal ganglion cell

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51
Q

where r intrinsically photosensitive RG cells (ipRGC) located + why

A
  1. mostly located on lower 2/3s of the retina
  2. this is bc blue light mainly comes thru sky, so wld mostly be hitting bottom of retina (looking @ blue light centre-on has biggest effect)
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52
Q

what do the signals of ipRGC do

A

signals sent 2 the brain govern production of cortisol (day) + melatonin (evening n night)

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53
Q

what photopigment do ipRGC use + where do their axons project 2

A
  1. use photopigment melanopsin (this is maximally sensitive 2 blue light)
  2. axons project 2 the suprachiasmatic nucleus (SCN) instead of image-forming parts of brain
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54
Q

synaptic transmission - what happens !

A

nerve impulse (electrical signal) arrives @ presynaptic terminal
→ drives voltage-gated calcium channel 2 open, calcium flows in
→ synaptic vesicle fuses w membrane + NTs r released (chemical signal) on2 the NT receptor
→ bind 2 NT receptor on postsynaptic cell
→ once vesicle content has been spilled out, pulled back up in2 synaptic terminal + loaded w NTs, stored until new AP arrives

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55
Q

the main excitatory NT in nervous system is glutamate . describe it/what it does

A
  1. it’s an amino acid
  2. once released, binds 2 receptors sensitive 2 it (many have ion channels)
    → ion channels open, Na+ flows in2 cell
    → causes depolarisation of postsynaptic cell, results in EPSP
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56
Q

main inhibitory NT is GABA . what does it do

A

binds 2 GABA receptors (often attached 2 Ka+ channels)
–> Ka+ flows out, inside of cell becomes even more negative than b4 (hyperpolarisation of membrane)
–> inhibitory postsynaptic potential (IPSP; less likely 4 neuron 2 fire)

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57
Q

in which 3 layers of the eye does depolarisation take place (in a flow-y way)

A

RGCs, bipolar cells, + photocreceptors r all glutamatergic/releasing glutamate)

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58
Q

which cells in the eye release GABA/ r inhibitory

A

horizontal + amacrine cells release GABA
→ inhibits synapses 2 their left + right (lateral spread of inhibition)

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59
Q

is lateral inhibition an opponent process (and what is an opponent process)

A
  1. yaa
  2. opponent process is when 2 nervous system processes r Competing
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60
Q

how does simultaneous contrast work (in this example, 2 squares - one has light background, one has dark)

A
  1. one w lighter background triggers activation of more cones sending signals
    → greater lateral inhibition (via GABA-producing cells)
    → will appear darker, bc competing neighbouring cones will b less active
  2. darker background:
    losing activation bc less light hitting eyeballs, so less lateral inhibition
    → perceived as lighter in colour
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61
Q

what’s another example of lateral inhibition/opponent processes in visual system

A

Mach bands !

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62
Q

we (humans) can see between 400-700nm wavelengths… what do these signify (ultraviolet etc)

A

we can see colours between ultraviolet n infrared

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63
Q

what type of wavelengths r more damaging

A

shorter wavelengths w higher frequency (e.g. gamma ray, x-ray)

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64
Q

what is the opponent-process theory 4 colour perception

A

colour perception controlled by activity of 2 opponent systems (yellow-blue mechanism, red-green mechanism)

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65
Q

what colour cones r blue cones opposed 2

A

opposed 2 red + green (yellow)
→ attempts 2 inhibit yellow
→ blue colour after-image when u look @ smh yellow n vice versa

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66
Q

example of opponent processes in motivation

A

approach-avoidance conflict arises frm competition 2 pursue reward vs. 2 avoid harm

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67
Q

snakes, rats, + mice. what vision type do they have

A

monochromatic

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68
Q

most mammals have dichromatic vision.. what does this mean

A

seeing only blues n greens

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69
Q

humans, apes, + old world monkeys - what type vision do we have?

A

trichromatic - greens, blues, reds

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70
Q

how many photoreceptor types do birds, reptiles, + fish often have

A

Four

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71
Q

how many colour receptors do mantis shrimp have

A

12 !! (8 in the visible spectrum, 4 in the UV)

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72
Q

approx. 5-10% of males + 0.1% females r which type of colour blind

A

red/green

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73
Q

most common type of colour-blindness ..? (1st and 2nd)

A
  1. weak in green vision (a.k.a. deuteranomaly)
  2. no red (protanopia)
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74
Q

how r images projected on2 the retina

A

images r projected inversely (upside down) on2 retina

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75
Q

when do on-centre, off-surround LGN cells fire

A

when light is shone right across centre of receptive field (if light shines on periphery, it inhibits activity of the cell)

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76
Q

wld on-centre, off-surround LGN cells fire if light bar was shining in2 centre AND surround

A

no, no change in firing

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77
Q

r simple V1 cells monoclular of binocular

A

can b either

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78
Q

what does a simple cell in V1 respond 2 best

A
  1. elongated bars or edges of objects (Not dots)
  2. orientation selective (e.g. cld be sensitive 2 diagonal light bars)
  3. have separate on + off subregions (matters where in visual field bar is presented)
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79
Q

V1 complex cells are..? and have..?

A
  1. orientation selective
  2. nearly all binocular
  3. have spatially homogeneous receptive fields (no on/off subregions)
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80
Q

columnar architecture of V1. describe this

A

as u move deeper in2 cortex, receptive fields + orientation preference of cells r maintained (orientation columns)
→ that is, all cells in one column as u go down might b receptive 4 same area, have preference 4 same orientation

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81
Q

s u go across V1 cortex (instead of deeper), what do u see?

A

see gradual change in spatial + orientation preference

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82
Q

retinotopy

A

remapping of retinal image onto cortical surface

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83
Q

which region of the eye uses more of V1

A

foveal region (greater magnification factor)

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84
Q

retinotopic mapping is an example of What type of organisation

A

topographic
–> that is, ordered representation of the sensory enviro where spatially adjacent regions (in the physical world) r represented in adjacent positions in the brain
(e.g., tones that r close in pitch r processed by close-2gether regions)

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85
Q

why does V1 use topography (overall + more specifically)

A
  1. clusters neurons w dense connectivity 2gether
    –> reduces axon length
    –> reduces axon volume (which brain volume is largely driven by)
    –> allows for more space 4 neurons + conserves metabolic resources
  2. facilitates lateral inhibition (if u have inhibitory cells spreading axons laterally 2 inhibit neighbouring cells, want them 2 not have 2 spread too far)
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86
Q

when pressure pulses r close together, is the sound frequency high or low

A

closer 2gether the pressure pulses r, higher the frequency measured in Hertz (Hz; 1 per second)

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87
Q

pressure pulses travel @ approx. 340 metres per second . T or F?

A

Trueee

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88
Q

humans can hear 20-20,000 Hz. T or F?

A

true

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89
Q

how many HZ can chickens hear between

A

100-2,000

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90
Q

how many HZ can bats hear between

A

10,000-100,000

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91
Q

how many HZ can dogs hear between

A

64-44,000

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92
Q

how many HZ can cats hear between

A

55-77,000

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93
Q

age-related hearing loss - who is most vulnerable + what goes first

A
  1. women do a little better w/ hearing thru-out ages
  2. lose ability 2 pick up on highest frequencies first
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94
Q

2 types of hair cells in ear: inner and outer (describe each briefly)

A
  1. inner hair cells transmit mechanical disturbance of membrane in2 electrical signals sent 2 the brain
  2. outer hair cells receive info frm the brain
    –> may contract w/ info, pulling tectorial n basilar membranes 2gether
    –> get depolarised, meaning stronger signals sent 2 brain
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95
Q

transduction def

A

conversion of sound 2 an equivalent electrical waveform

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96
Q

pathway 2 auditory cortex

A

cochlea
→ brainstem
→ midbrain (inferior colliculus)
→ medial geniculate nucleus (in thalamus)
→ auditory cortex

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97
Q

describe secondary auditory cortex (A2)

A
  1. important 4 sound localisation + analysis of complex sounds
  2. not necessarily tonotopically organised
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98
Q

why tonotopic organisation in A1?

A
  1. saves space + time (like retinotopic)
  2. allows sound 2 b encoded on the basis of time/frequency changes
    –> e.g. wld want to be able to distinguish frm low tiger growl + high-pitched bird chirping
  3. allows u 2 parse out certain frequency bands (scene analysis)
    –> e.g. being able 2 clap on beat by dismissing irrelevant frequencies
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99
Q

what is the benefit of beat detection (that tonotopic organisation facilitates)

A

promotes social cohesion

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100
Q

how else is beat detected/ other frequencies weakened

A

some medial geniculate neurons respond 2 the low frequency components
–> modulate firing threshold in A1 according 2 the underlying rhythm
–> responses that occur out of beat r then weakened

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101
Q

abt 6% of input 2 visual cortex is top-down (most bottom-up). is this statement true?

A

well yes !

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102
Q

top-down influences on auditory processing

A

while A1 is larger in macaques than humans,, surrounding areas (belt/A2 + parable) in humans r abt 10x larger
–>
so, most connectivity in2 human A1 is actually top-down (around 66% frm other cortical areas)

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103
Q

benefits of top-down influences on auditory processing

A
  1. allows context + procedural demands 2 bias perception (esp w similar frequency words)
  2. better predictive ability
    Greater integration of multisensory input
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104
Q

egocentric space def

A

YOUR relation 2 stuff in space

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105
Q

describe where the dorsal vs. ventral stream r frm V1

A

dorsal = top of brain, like fin on shark; ventral = straight across

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106
Q

humans have face recognition cells. when can u see/examine them?

A

when ppl r under surgery….

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107
Q

Quiroga et al. (2005) - what did they find

A
  1. found ppl w cells responding 2 Jennifer Aniston - didn’t matter what angle face was presented, cells wld keep firing
  2. this was the 1st demonstration of face-selective cells in humans!!
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108
Q

Ppl tried 2 follow on frm Quiroga et al.’s study n find cells similar 2 Jennifer Aniston cells. They succeeded in finding Halle Berry cells. How do these work?

A

Halle Berry cells fire regardless of partial occlusion of face or using a drawing instead of photo, can put words ‘Halle Berry’ on screen + got neurons firing
→
not facial recognition, but cortical representation of the idea of Halle

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109
Q

the Quiroga results display invariance. what does this mean ?

A

invariance in this context means encoding a representation so that it’s identified regardless of size, orientation etc. (cells respond in same way)

110
Q

so,,, do we just have special face cells? nothing else?

A

no!! we have architecturally discriminating cells (e.g. Eiffel Tower cell)

111
Q

cld cell firing b modulated by familiarity? (study)

A
  1. famous ppl don’t trigger that huge a shift in cells, relative 2 someone ur familiar w (e.g. brother, mother)
  2. BUT cells most triggered when presented w imag eof some1 recently encountered (e.g. experimenter)
112
Q

cld the firing of human ‘face’ cells b an emotional response? (study)

A

presented participants w ‘scary’ things - but didn’t generate cell reaction

113
Q

‘face’ cells cld b an example of grandmother/gnostic cells . what r grandmother cells?

A

grandmother/gnostic cells do local coding - so u have 1 highly localised cell 2 represent a given concept

114
Q

benefits of gma cells/local coding :

A

assists w discrimination between objects - cells either active during context A or context B

115
Q

why might the local coding theory not b an accurate explanation 4 ‘face’ cells (key reasons)

A
  1. requires huge number of gnostic units (need cell 4 every person u meet, every object u encounter)
  2. susceptible 2 damage (if ur Jen Aniston cell dies, wouldn’t b able 2 recognise her again) 3. generalisation is difficult - how can u solely identify Jen + not just ppl who look like her w/ only one cell?
116
Q

how many neurons in human brain (how many in hippocampus esp)

A

86 billion neurons overall, 40 million in hippocampus

117
Q

the 3 critical goals of visual processing are to:

A
  1. separate patterns
  2. complete patterns - so u have complete mental picture
  3. generalise - use past info 2 recognise things
118
Q

dense (ensemble, population, distributed) encoding theory - alternative explanation 4 ‘face’ cells

A
  1. don’t have single cell representing item
  2. have diff population of cells encoding distinct things that have smth 2 do w item (e.g. looking @ ur mother, some cells will fire 4 hair + some 4 teeth)
  3. cells all fire 2gether to give item representation
  4. there IS some overlap tho,, which is a detractor 2 the theory
119
Q

what is distributed encoding (beyond it being a mix of local + dense encoding)

A

in distributed encoding u have:
certain cells devoted 2 a specific context + other cells that r active in response 2 features shared by both (or more) contexts
→
therefore get sparseness needed 2 generare separate representations, while having sufficient overlap 2 get generalisation + pattern completion

120
Q

what is principal component analysis

A

simplifies large amounts of data while maintaining important trends etc.

121
Q

what did Doris Tsao do (finding evidence 4 distributed facial representation code)

A
  1. identified 50 dimensions that varied most across faces (25 for shape, 25 for appearance)
  2. manipulated images 2 get new faces along any of these 50 diff dimensions (e.g. might change shading)
  3. recorded cell activity in the middle lateral, middle fundus, + anterior medial ‘face patches’ when participants presented w images on screen
122
Q

what did Tsao find

A

found:
1. specific cells respond when one dimension in particular has been altered
2. single cells r tuned 2 one axis of face space + r blind 2 changes orthogonal 2 this axis
3. AND when she reconstructed faces frm the firing activity of 205 neurons, Tsao found vv accurate face predictions !!

123
Q

what’s important abt Donald Hebb (1904-1985) . speak Broadly

A
  1. thought abt how a series of interconnected cells could possibly store info
  2. heavily influenced fields of neurosci, computational science
124
Q

in order 2 prove LTP is a mechanism 4 learning, u need to show..:

A
  1. show that blocking LTP prevents memory formation
  2. show that reversal of LTP produces forgetting
  3. show that learning leads 2 LTP-like changes
  4. show that producing LTP creates false memories or masks existing memories (v difficult/impossible 2 do)
125
Q

LTP requires activation of NMDA subtype of glutamate receptor . T or F?

A

true duh

126
Q

AP5/APV selectively block NMDA receptor. T or F..?

A

True

127
Q

LTP maintenance can be prevented by the drug ZIP (zeta-inhibitory peptide). T or F?

A

True

128
Q

V1 is for orientation (largely), V4 is for colour perception, + V5/MT is 4 motion detection . T or F?

A

true

129
Q

Patient M.P. had bilateral lesions of V5. T or F?

A

True

130
Q

how was patient M.P. impaired

A

motion perception was drastically impaired (saw things like slowed-down frames), while colour perception, etc. remained fine

131
Q

all cells in V5 have direction tuning ..what does this mean?

A

only fire when stimuli move in a certain direction

132
Q

V5 cells r also tuned 2 things moving @ specific speeds . T or F?

A

T

133
Q

optic flow def

A

looks like whole world is moving as u move thru it

134
Q

looming def

A

detection of change in visual angle as you approach an object (object expands + becomes bigger)

135
Q

what is the binding problem

A

challenge of preventing the properties of one object representation frm being mistakenly assigned 2 another

136
Q

temporal binding (possible solution 4 how brain recognises features of one object as belonging 2 That object): how does it work?

A

cells firing in synchrony form cell assemblies that collectively represent a given object @ a moment in time
–>
this shared timing tags specific cells as sharing the same ‘message’ + links the features of an object together

137
Q

what was Karl Lashley (psychologist)’s theory of the biological seat of memory, and how did he get there (hint: rats and Maze)

A
  1. trained rats on maze (had 2 remember how 2 complete task 2 escape + get reward)
    → lesioned specific parts of the cortex 2 see effect on memory
    → didn’t find any part that wld significantly affect memory
  2. Ultimately, decided there was no single area of cortex devoted 2 storing memories
    → all parts of cortex equally capable of storing memories (equipotentiality)
    → principle of mass action (cortex as a whole stores memories - so, bigger the lesion, greater the chance of memory impairment)
138
Q

in 1953, H.M. Trashed Lashley’s theory. yes or no?

A

yess

139
Q

describe H.M.’s case (also,, Scoville was his surgeon) - how did he disprove Lashley’s theory

A
  1. suffered frm temporal lobe epilepsy
    →
    got bilateral temporal lobectomy, during which 50-60% of each hippocampus was removed (along w a lot of adjacent cortex)
    →
    then developed severe anterograde amnesia + retrograde amnesia going back a yr or 2 prior to surgery (all recently acquired memories lost)
    →
    cldn’t remember certain episodes but cld obtain Some new memories (acquired mirror drawing task, although didn’t remember being trained on it - source amnesia)
  2. soo,,, bc he cld form short-term memories (20-30s) but not long-term ones, there is evidence 4 hippocampus being involved in memory consolidation
140
Q

semantic memory def

A

facts

141
Q

episodic memory

A

memory of (life) events

p.s. H.M. had severe amnesia 4 episodic memories, while semantic memory was less affected

142
Q

disrupting the hippocampal circuit: patient R.B.

A

had an ischemic event which temporarily stopped blood supply 2 brain
→ resulted in damage 2 the CA1 area (in hippocampus)
→ marked anterograde amnesia + minor retrograde amnesia

Rey-Osterrieth test: R.B. cld copy image when in front of him, but did poorly on reproducing image w/ out seeing it in front of him
→ control w no hippocampal damage performed fine when image was taken away
→ CA1 region especially important (+ wider hippocampus) 4 formation + storage of memories

143
Q

ischemic event def

A

loss of blood supply - heart attack or stroke

144
Q

Rey-Osterrieth figure test

A

get presented w image + asked to copy it (first when it remains in front of subject, then after it’s been taken away)

145
Q

rhinal cortex def

A

portion of cortex below/ventral 2 hippocampus, major site of input to hippocampus

p.s. Scoville went thru rhinal cortex when performing surgery on H.M. ….

146
Q

diencephalic amnesia characterised by..?

A

deficits in anterograde memory (?) + retrograde amnesia, w preserved motor learning

147
Q

patient N.A. - what’s their story ?

A

penetrated thru mammillary body 2 anterior area of thalamus (medial dorsal thalamus)
- important 2 note this is all connected 2 output area of hippocampus
→
ended up w diencephalic amnesia, memory deficits similar 2 H.M. (severe declarative memory deficits)

148
Q

Wernicke-Korsakoff Syndrome or ‘wet brain’ or ‘Beriberi’

A
  1. alc has consequences on nutrition, become lacking in thiamine (vit B1)
    → end up w similar memory deficits 2 H.M. (or someone w temporal lobe damage)
    → mamillary bodies damaged (receive input frm hippocampus) + also dorsal medial nucleus of thalamus
    → IQ memory scores significantly lower
  2. amnesia due 2 heavy drinking basically …
149
Q

paired associates memory test (show word pairs, take them away, then ask what they were paired w): how do ppl w temporal lobe damage perform

A
  1. everyone w temporal lobe damage performs vv poorly
  2. alcoholics might have reduced performance compared 2 non-alcoholic controls
150
Q

specific episodic memory task (how many items frm a story can u repeat back): how do alcoholics perform?

A

ppl w alcoholism perform slightly worse than non-alcoholics, but still wayy better than ppl w temporal lobe damage

151
Q
A
152
Q

where does binding of info occurs 2 create one whole memory

A

in input stages frm cortex 2 hippocampus

153
Q

give an overview of the hippocampal diencephalic memory system

A

amygdala receives hippocampus input → projects 2 hypothalamus (involved in emotional signalling)

154
Q

what shld damage 2 the hippocampal diencephalic memory circuit produce ?

A
  1. deficits like in H.M.
  2. BUT remote memories (1-2 years+) don’t depend on this circuit in the same way
155
Q

why don’t 1-2 yrs+ memories depend as much on the hippocampal diencephalic memory circuit

A

when ur forming memories, info gets bound in hippocampus
–>
after a while, memories become independent of circuit + r stored long term in distributed networks across the cortex

156
Q

Lashley didn’t go deep in2 brain, lesioning superficial areas - that’s why he didn’t find shit . if he hit cingulate gyrus, would he have found impact on memory

A

yes, he would’ve

157
Q

what encodes the ‘where’ aspect of episodic memory

A

hippocampus
–>
u can see this in the Morris Water Maze results (animal w lesioned hippocampus starts swimming ‘round in circles, unable 2 locate platform –> spatial memory dependent on hippocampus)

158
Q

allocentric reference def

A

looking @ where everything else is
- e.g. using east or west to locate people (external world)

159
Q

water maze results (variable start/allocentric point of reference)

A

rats w lesioned hippocampi Can’t learn → hippocampus v important 4 allocentric representations of space

160
Q

water maze results (egocentric point of reference - starting in same place each time)

A

rats w lesioned hippocampi took longer 2 learn than controls
→ after 12 trials, performance is abt the same

161
Q

takes 4 yrs of training 2 learn London’s 25k streets . T or F

A

true

162
Q

cabby driver vs. control (hippocampus volume)

A

increased posterior hippocampal volume in taxi drivers compared 2 controls,, decrease in anterior portion

163
Q

comparing hippocampi of taxi vs bus drivers

A
  1. increased posterior volume in cabbies only
  2. taxi drivers performed worse on Rey-Osterrieth complex figure test
164
Q

receptive field of hippocampal place cells? what do these place cells do

A
  1. have receptive field that is some area of space - fire selectively when person is @ a certain point in space
    →
    can give u a tiled representation of ur entire spatial surroundings
  2. ALSO there’s a subset of hippocampal cells firing 4 any location - pattern of activity cld b incorporated in2 a memory representation + might underlie the ‘where’ of episodic memory
165
Q

chronoception

A

study of time perception (subjective experience of time)

166
Q

time production experiment (THC)

A

might tell some1 to hold down mouse button for a few seconds (5-30), then time how long they hold it down
→ even low doses of THC cause ppl 2 hold down button 4 less time

167
Q

time estimation experiment (THC)

A

give some1 task + ask how long task took
→
controls experienced no effect on time perception, but even low dose of THC makes time estimation much higher

168
Q

SCAD (suspended catch air device) study - go 2 v high platform, fall + r caught by net → time seems to slow . detail this further

A

b4 participating in fall, estimated fall duration not that much (2s)
–>
after participating in fall, estimated fall duration seems much longer (3s)

169
Q

chronostasis def + example in vision

A
  1. halting of time
  2. when u shift gaze rapidly frm one point of fixation 2 another ur visual system suppresses info frm retina during that shift
    →
    brain has 2 then fill in blanks 4 that period of time (usually decides it was seeing its new point of fixation 4 the past ms)
170
Q

flash lag illusion explained

A

neither red nor blue square is larger, NS is locating the squares forwards in time (i.e. where they Will be in the future)

171
Q

Scalar Expectancy Theory (SET) model of timing

A

have pacemaker (generating pulses in brain), when event occurs a switch activates a time stamp
→ accumulate more cycles/pulses of pacemaker (longer event goes on, more cycles u accumulate that r stored in short term memory) → compared 2 long term memory template

172
Q

if u speed up pacemaker but keep the same chronological time, cld have smth like 4.5 cycles to 3 seconds (as opposed to 3 cycles to 3s)… what time estimation wld this lead 2

A

4.5 second estimation

173
Q

what cld pacemaker b in brain?

A
  1. neural trajectories (reproducible sequence of activation w/ in a population of neurons)
    → cld have specific cells firing @ a particular point in time
    → if u want 2 increase speed that time appears 2 pass cld speed up sequence of cell firing
  2. ramping up
    → as u get closer in time 2 goal (e.g. getting gift), cld have a broadening in neuron firing rate
174
Q

hippocampal time cells (found decade ago) r capable of what..? + also what is evidence 4 them existing

A
  1. representing passage of time
  2. rats need 2 navigate arena 2 get reward
    →
    electrodes implanted in hippocampus (while rat is stationary in terms of spatial location - no place cells involved)
    →
    as time passes, sequence of cells that fire in hippocampus (evidence of time cells)
175
Q

humans normally good @ estimating period of time of up to at least 20s . T or F

A

T

176
Q

interval reproduction study (asked H.M. + control group 2 estimate amt of time that command took) … results?

A
  1. control good @ estimation, H.M. Not
  2. as u increase period of true time, trend continues w H.M. perceiving more time than there was
177
Q

see other ppl w temporal lobe amnesia also having time perception issues (Buzsaki & Llinas, 2017)

A
  1. took controls + ppl w temporal lobe amnesia on tour of their facility
  2. @ each time point, certain things happened (e.g. someone dropping smth on the floor)
  3. asked to regurgitate memory of whole tour
  4. ppl w temporal lobe amnesia reported fewer episodes AND their sequence of events was completely jumbled up
178
Q

valence def

A

positive or negative emotional value ascribed 2 memories

179
Q

Memory for 9/11 study

A
  1. had 2 groups - downtown (close to site) + midtown (farther away)
  2. asked them 3 yrs after event 2 report their memory of that day
  3. downtown group had strong memory of 9/11,, midtown not sm
    → closer u were 2 twin towers, stronger ur recall of that day
  4. also asked 2 recall memories of previous summer
    → way better recall 4 9/11 than previous summer 4 downtown group
180
Q

lecture material is better remembered after post-lecture arousal. evidence?

A
  1. given mini test 2 weeks after lectures finished
  2. lectures days 1 + 3 identical, day 2 they showed groups 2 diff videos (control given boring video, experimental given graphic clip of oral surgery)
  3. students shown graphic video had better recall of day 2 lecture than controls
181
Q

CNS stimulants can enhance memory if timing is right. evidence?

A

memory is enhanced by administration of low doses of CNS stimulants 2 rodents shortly after training,, but not after a delay period (has 2 b during or just after task)

182
Q

where r adrenaline/epinephrine + cortisol produced

A

adrenal gland

183
Q

adrenaline is both a hormone + NT (difference is target organs) .. elaborate a bit

A
  1. hormones released by gland somewhere in endocrine system shld b acting on diff organ system
  2. NTs shld b acting specifically on neural cell types
184
Q

where is adrenaline released + what controls its release

A
  1. adrenaline released by adrenal medulla (inner portion of the adrenal gland) which regulates + secretes adrenaline in response 2 stress
  2. release is controlled by the hypothalamic-pituitary-adrenal (HPA) axis
185
Q

can adrenaline cross BBB

A

adrenaline doesn’t cross the BBB well
–>
therefore,, influences the brain via activation (as a NT) of the vagus nerve
–> spike in adrenaline activates vagus nerve, which sends Quick signal 2 brain

186
Q

vagus nerve def

A
  1. nerve that runs frm brainstem to peripheral organs
  2. sends + receives signals frm organs
187
Q

When is cortisol known as when used as medication

A

Hydrocortisone

188
Q

Can cortisol cross BBB easily

A

Yes

189
Q

what is cortisol, what processes is it involved in

A
  1. steroid hormone, initially formed frm cholesterol
  2. involved in processes including metabolism + immune response
190
Q

cortisol is released by HPA axis. describe this more

A

hypothalamus releases hormone CRH
→ acts on cells in pituitary gland → causes release of hormone ACTH into the blood
→ adrenal glands
→ glands release cortisol
→ eventually gives u adrenaline

191
Q

amygdala activity during film viewing correlates with recall 3 weeks later . give more details

A

positive correlation between use of glucose in amygdala + no. of short films u can recall seeing if ur shown emotional films
→
strong correlation between emotional memory + amygdala function (bc basolateral amygdala sends heavy projections 2 hippocampus)

192
Q

slow cortisol release doesn’t seem beneficial 4 memory … how does the Yerkes-Dodson Law come in here

A

well: lil bit of stress good 4 u (thru adrenaline route),, but ongoing stress damages ability 2 retain memory (cortisol route)

193
Q

Do both quick (adrenaline) + slow (cortisol) ways that stress hormones act activate the amygdala

A

Yes, which in turn activates hippocampus

194
Q

Alzheimer’s disease most common form of dementia. give a brief definition of dementia

A

when a person experiences gradual loss of brain function due 2 physical changes in brain

195
Q

what causes dementia

A
  1. Alzheimer’s
  2. vascular dementia (e.g. after stroke, loss of nerons in damaged area)
  3. Lewy body dementia (build up of proteins in2 masses known as Lewy bodies)
    frontotemporal dementia (degradation in frontal + temporal lobes)
196
Q

stressor effects on memory are mediated by the amygdala (rat study) …

A
  1. had controls + rats injected w amphetamine in the amygdala (amphetamine boosts amygdala activity)
  2. two conditions 4 amphetamines:
    one group immediately injected, other is 2hrs after final training trial
  3. only rats given immediate amphetamine injection much quicker 2 find platform
    –>
    soo boosting activity of amygdala soon after learning smth boosts retention of memory
197
Q

what is the prognosis 4 Alzheimer’s

A

6-10 yrs

198
Q

describe what tests u can do 4 Alzheimer’s … phonemic + semantic verbal fluency (SVF)….

A
  1. phonemic fluency - tell me as many words as u can in 1 min starting w letter ‘b’
  2. semantic fluency - tell me as many animals as u can in 1 min

measure no. of correct words

199
Q

prevalence of Alzheimer’s by age group

A
  1. up until 60, 1-2% of global pop.
  2. once ur 65, likelihood of developing condition doubles every 5 years
  3. @ 85 have approx. 20% prevalence (NZ)
200
Q

how many cases of Alzheimer’s rn

A
  1. approx. 50 million
    –> on course 2 overtake stroke + heart attack economic burden combined
201
Q

brain changes in Alzheimer’s

A
  1. extreme shrinkage of cerebral cortex
  2. extreme shrinkage of hippocampus
  3. severely enlarged ventricles
  4. loss of cholinergic projection neurons of the basal forebrain (part of the arousal system, can help u learn)
    →
    ACh (acetylcholine; pro-memory signal, boosts LTP) lost w Alzheimer’s
202
Q

normally ACh carries a message across the synapse, then is broken down by cholinesterase → taken back up in the form of choline … how can u use ACh 2 improve Alzheimer’s symptoms

A

y using cholinesterase inhibitors (only useful 4 mild 2 moderate conditions), the ACh continues 2 float around
→
gives it time 2 time transmit messages, helps w Alzheimer’s symptoms

203
Q

list some cholinesterase inhibitors

A

Donepezil (Aricept)
Rivastigmine (Exelon)
Reminyl (Galantamine)

204
Q

what r some Horrors (biologically) that r associated/may cause Alzheimer’s

A
  1. plaques - aggregates of protein beta-amyloid, clump 2gether outside of cells (impair synaptic function)
  2. neurofibrillary tangles - aggregates of tau protein (clumps of proteins that group 2gether inside cell)
205
Q

Amyloid precursor protein (APP) is a protein w an important role in synaptic plasticity. T or F?

A

true

206
Q

how is beta-amyloid produced (bearing in mind over-production of beta-amyloid is associated w Alzheimer’s)

A

beta-secretase + gamma-secretase cleave APP protein → beta amyloid produced

207
Q

what prevents beta-amyloid formation

A

prevented by alpha secretase cleaving APP protei

208
Q

Aducanumab - antibody against beta-amyloid formation (monoclonal antibody) . was/is it useful 4 AD

A

no !

209
Q

does beta-amyloid plaque location map on2 symptoms well..?

A

no,, some ppl have lots of beta-amyloid plaques w no AD symptoms

210
Q

why was study on beta-amyloid oligomer AB*56 published in Nature (2006) fraudulent

A

used western blotting
→ each horizontal line shld represent diff protein, but expanded image shows that the lines look the same in terms of shape
→ only possible thru photoshop (FALSIFIED DATA)

211
Q

western blotting def

A

gel that u put proteins into, then apply a charge 2 gel
→ proteins moved by electrostatic force
→ get a separation of proteins thru-out gel depending on weight

212
Q

what does Donanemab (antibody, came out in 2023) do

A
  1. radio-labelled amyloid plaques across 76 weeks (people either given antibody or placebo)
    →
    plaques broken down by antibody Donanemab
  2. cognitive decline was slowed by approx. 35% over 18 months
213
Q

in a healthy neuron, there’s a scaffold (cytoskeleton) that the cell is built around . how does tau protein relate 2 this

A

scaffold made up of microtubules (tightly wrapped coil of proteins that give cell structure), tau protein normally sits on outside of microtubules (helps bind little proteins 2gether)

214
Q

in AD, tau proteins leave the microtubules … what happens next?

A

they become hypo-phosphorylated (lots of phosphate being added 2 tau protein)
→ no longer able 2 bind as tightly, so let go
→ this causes microtubules 2 disintegrate, impacts on neuron health
→ get tau protein just floating around, forming clumps inside cell

215
Q

tau protein buildup maps onto AD symptoms wayy better than beta amyloid . T or F?

A

true

216
Q

Braak stages (Tau protein)

A
  1. tau protein 1st starts 2 show signs of aggregating in medial temporal lobe (start off in transentorhinal region)
  2. tangles spreading thru entorhinal cortex + starting 2 b visible in hippocampus
  3. get lots more tau deposition, not just in cortex + hippocampus but in other areas of cortex too
217
Q

what r ur chances of developing early-onset AD if one of ur parents has it + what mutations is it linked 2

A
  1. 50%
  2. mutation on PSEN1, PSEN2, APP genes
218
Q

early-onset AD (present @ less than 65 yrs; mostly familial, not necessarily genetic) makes up what percentage of total AD cases

A

5%

219
Q

what doe astrocytes do (that’s relevant here)

A

take stuff frm blood supply + put on2 neuron 2 provide metabolic support

220
Q

late-onset AD (sporadic, 95% of cases) … what is risk related 2

A

related 2 variations of the APOE gene on the chromosome 19
→ 3 major variations/alleles of gene: APOE2, APOE3, APOE4
→ everyone born w 2 alleles of the gene, around 2-5% of pop. carry 2 copies of the E4 allele
→ 1 copy of E4 = 2-3 x higher risk of AD; 2 E4s = 5-8 x higher risk

221
Q

what does APOE gene do

A

produces protein mainly found in astrocytes
→ protein transports cholesterol frm astrocytes 2 neurons

222
Q

how is APOE4 integral 2 BBB… start off by describing BBB

A
  1. endothelial cells make up external wall of capillary, have tight junctions that allow some things 2 pass + not others
    - outside endothelial cells have pericytes (regulate formation of tight junctions), then have layer of astrocytes
  2. APOE4 can disrupt formation of tight junctions, opening up BBB (making it leaky)
    →
    selectively impairs function of pericytes
223
Q

what r endothelial cells

A

blood capillaries

224
Q

why does BBB exist

A

2 keep blood separate frm brain tissue (blod is toxic, has lots of iron)

225
Q

study looking @ people w APOE4 + their cognitive decline, level of pericyte injury… what were the results

A

gave ppl mental state exams @ 2 year intervals
–> rate of cognitive decline much steeper 4 individuals w higher levels of pericyte injury

226
Q

University of Minnesota ‘Nun Study’ (what might protect against AD): method

A
  1. 678 nun participants
  2. wrote early life autobiography @ average age 22
  3. looked @ how complex reports were (marker of cognitive performance), then looked @ ppl who had vs. didn’t have mild cognitive impairment or dementia (aged 75-102)
227
Q

University of Minnesota ‘Nun Study’ (what might protect against AD): findings

A

ppl w high density scores early in life (detailed accounts) associated w intact cognition later on, regardless of AD lesions

228
Q

what percentage of dementia cases worldwide are preventable

A

45%

229
Q

name the bits of our prefrontal cortex

A
  1. dorsolateral prefrontal cortex
  2. ventrolateral prefrontal cortex
  3. orbitofrontal cortex
  4. medial prefrontal cortex (inner part of prefrontal cortex)
  5. anterior cingulate cortex (ACC)
230
Q

lateral = out to the side; ventro = lower .
T or F?

A

true

231
Q

what damage dud Phineas Gage incur age 25

A

rod went thru skull, damaging ventromedial region of both frontal lobes + sparing dorsolateral

232
Q

classic working memory test/delayed response task

A

monkey first displaces sample object 2 get reward
→ after a delay, 2 objects r shown
→ recognition memory is tested by having monkey choose a new object that doesn’t match sample 2 get reward

233
Q

what does PFC cell firing look like during delayed response task

A

some PFC cells respond during the cue period + others during the delay period
→ firing of ‘delay cells’ cld maintain info in working memory
→ suggests that PFC is actively encoding info

234
Q

prefrontal lesions impair working memory performance (study)

A
  1. groups: VM damage, right DL/M damage, left DL/M damage
  2. for all, decreased performance in 60s
  3. all of prefrontal lesioned individuals had worse working memory performance compared 2 controls (esp right DL/M prefrontal cortex)
235
Q

n-back test (4 working memory)… describe

A
  1. presented w diff symbols on a screen, have 2 give signal when some kind of criterion has been met (e.g. tell me when b appears on screen)
  2. 1-back test - target is t, u need 2 signal when u see a t immediately followed by another t
    –>
    make things progressively more difficult (e.g. signal when there’s a b followed 3 frames later by other b)
236
Q

n-back test findings (PFC, lures)

A
  1. increased activity in PFC (dorsolateral) during task, esp when lures r presented
  2. working memory span associated w ability 2 suppress non-relevant info (lures)
237
Q

Tower of London test outline + what does brain-scanning during task show

A
  1. have initial configuration + target configuration (have to turn into target configuration in least number of moves)
  2. activation in PFC (esp in dorsolateral PFC, a.k.a. Brodmann Area 46)
238
Q

why is the PFC involved in working memory?

A

good bi-directional communication w structures of temporal lobe (involved in long-term memory)
→ can then make plan based on past experience + current context (getting direct sensory info)

239
Q

inhibitory (self-) control def

A

where previously reinforced, highly reinforcing, or well-learned (habitual) responses have 2 b suppressed

240
Q

successful self-regulation associated w top-down control frm the PFC over subcortical regions involved in reward + threat processing . T or F?

A

true

241
Q

hot/cool framework

A
  1. hot system
    - emotional, reflexive
    - develops early in childhood, accentuated by stress
    - might b some sort of stimulus which provokes that reaction
  2. cool system
    - using past experience 2 decide behaviour
    - comes on later in brain development, requires self-control
242
Q

utilisation behaviour (+ environmental dependency): guy w damaged PFC (studied by Lhermitte, 1983)

A

experimenter takes off glasses
→ patient sees them, picks them up, + puts them on his own head
→ utilisation behaviour (driven by a certain sensory stimulus)

243
Q

test of frontal lobe function: Wisconsin card sorting task

A

told 2 sort cards (not told how)
→ told sorting is either correct or incorrect - if incorrect, have 2 try new way
→ after a few correct attempts, change rule
→ ppl w PFC damage find it vvv difficult 2 switch to new rule, will persevere w old one
→ brain scan shows in controls PFC becomes more active as task gets more complex (esp dorsolateral PFC)

244
Q

Performance in a go/no go task (impulsivity): method

A
  1. Followed ppl up 40 yrs after Mischel’s marshmallow task (divided in2 low + high delayers)
  2. Shown faces, told 2 sort by sex
  3. Cool task = neutral faces; hot task = emotional faces
245
Q

Performance in a go/no go task (impulsivity): results

A
  1. false alarm rate higher 4 low delayers
    →
    delayed gratification @ 4 yrs old indicative of impulsivity later in life
  2. ## brain scan showed:if u correctly inhibited response, there was significant activation in right inferior frontal gyrus (in PFC)
    -
    low delayers had greater activity in ventral striatum (dopamine neuron hub, reward surge) when inhibiting responses 2 happy faces
246
Q

self-control (Dunedin Study)

A
  1. self-control assessed between age 3-11, adult outcomes assessed at 32
  2. have childhood self-control scores plotted against adult criminal conviction
  3. low (score of 1) childhood self-control associated w an approx. 45% chance of having criminal conviction by 32
247
Q

how does effortful training work + does it boost self-control

A
  1. specific focus on attention + working memory
  2. usefulness: seems 2 b selective to task, limited generalisation
248
Q

How does effortless training work + does it boost self-control

A
  1. Mindfulness, flow states, nature exposure
  2. Useful ! works !!
249
Q

set shifting (changing strategy ur using): trail-making test

A
  1. Part A: asked to move from diff positions, then join up dots
  2. Part B: go again in sequence, but alternating between numbers + letters
  3. score correlates w dorsal PFC thickness
250
Q

why is dorsolateral PFC so involved?

A

connected 2 motor structures + parietal/occipital visual association areas (involved in movement relating 2 objects in space)
→
can therefore integrate info + put action plan/movement into place

251
Q

concrete thinking

A

reasoning that’s based on present experience

252
Q

name some ways 2 test 4 abstract thought

A
  1. Raven’s Progressive Matrices
  2. delayed match-to-sampling task
  3. proverb interpretation
253
Q

describe Raven’s Progressive Matrices (test of non-verbal reasoning, abstract thought)

A
  1. stages: matching, figural, analytical (requires most abstraction)
  2. brain activity during task: during analytical stage there’s lots of DLPFC activity
    → abstraction cld b dependent on DLPFC
254
Q

delayed match-to-sampling task: looking @ the neurons in monkey DLPFC

A
  1. implanted electrodes in DLPFC, paired presentation of sample w particular cue (e.g. certain tone)
  2. e.g. of idea: if u hear certain tone, need 2 obey non-match rule; if certain tone not present, obey match rule
  3. results: DLPFC fired regardless of what rule was 2 b followed → cld point 2 existence of general rule cells ?
255
Q

individuals who make the most concrete errors while interpreting proverbs r those w damage 2 the left lateral PFC .. what r examples of these concrete errors

A

for the proverb ‘Rome wasn’t built in a day’, a concrete error might be ‘Rome is a beautiful city’

256
Q

what’s the proposed anterior-posterior organisation of PFC

A

further anterior (front) u go, more cells u get w abstract thought

257
Q

action hierarchy

A

all the things u need in place to achieve ultimate goal

258
Q

cognitive control during planning + execution involves:

A
  1. identifying primary + subgoals
  2. retrieval + selection of relevant info
  3. simultaneously maintaining multiple subgoals
  4. determining what’s required 2 achieve goals
  5. anticipating consequences
259
Q

VMPFC lesions + ability 2 organise behaviour: multiple errands study

A

individuals who performed worse had VMPFC damage (as compared 2 controls, ppl w other damage 2 brain, + ppl w other PFC damage)
→
so,, PFC involved in rule following
→
cld b constraining creative thoughts? (spoiler: no)

260
Q

prefrontal lesions + the ability 2 organise behaviour: multiple errands test

A
  1. looked @ individuals w frontal lobe damage
  2. gave them 8 tasks, 6 of which were simple
  3. 7th required some future planning, 8th difficult
  4. individuals w frontal damage couldn’t plan v well, got confused
    →
    overall less economical way of completing tasks
261
Q

sculpting the response space def

A

role of DLPFC 2 define a set of responses suitable 4 a particular task n then bias these 4 selection

262
Q

study where u make the following problems true by moving 1 stick … (what r the results 4 ppl w lateral PFC damage)

A
  1. 3 problems, for 3rd one u have 2 come up w an atypical strategy + discard rule
    –> ppl w lateral PFC damage do better than controls on atypical problem
  2. 1st problem easy, both do well; 2nd hard, ppl w lateral PFC do worse
263
Q

with PFC damage, looking more @ ppl’s deficits than a sudden greater creative ability… provide an example

A

e.g. lack of inhibition (can’t stop drawing; perseveration)

264
Q

most patients w FTD have decrease in divergent thinking (which is integral 2 creativity). T or F?

A

true

265
Q

creativity-related performance: controls, patients w bvFTD (behavioural/frontal variant), + semantic/temporal dementia (SD)

A

from best 2 worse scores in creatifvity: controls → bvFTD → SD
→ ppl w frontal lobe damage not more creative

266
Q

Symptoms of frontal lobe syndrome

A
  1. Cognitive impairments (deficits in temporal ordering, poor decision-making → dysexecutive syndrome, etc.)
  2. Emotional changes (apathy, anergia, etc.)
  3. Behavioural deficits (utilisation behaviour, perseveration, environmental dependency, etc.)
267
Q

anergia def

A

lack of energy

268
Q

Balint syndrome causes + def

A
  1. Typically a bilateral lesion of the parietal lobe
  2. Can only perceive one object @ a time
269
Q

what damage is visuospatial neglect associated w

A

right parietal lesions

270
Q

signal detection task:
when u attend 2 stimulus + correctly perceive it being there (get hit), this is correlated to activity in …?

A

right lateral PFC

271
Q

signal detection task:
decision 2 act involves activation of… ?

A

medial PFC

272
Q

what part of the PFC is involved when ur biased (e.g. 2 respond ‘yes’)
left lateral PFC (damage affects ur bias, tied 2 perseverance?)

A

PSYC211 (5 decks)

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