Jones Flashcards
how long does it take u 2 make choice n execute command when choosing between 2 things
350-450ms
what makes up the CNS vs. peripheral nervous system (broad)
CNS = brain + spinal cord; peripheral nervous system (PNS) = everything else
what can the PNS b divided in2
- somatic nervous system - part of nervous system interacting w/ external enviro →
afferent n efferent nerves - autonomic nervous system (regulating body’s internal enviro)
→
afferent n efferent nerves (efferent nerves here further divide into parasympathetic n sympathetic nervous systems)
afferent vs. efferent nerves
afferent = input/info going in; efferent = output
parasympathetic vs. sympathetic nervous system
- parasympathetic: relaxation (‘rest + digest’)
- sympathetic: involved in physiological arousal (‘fight or flight’)
describe the 12 cranial nerves connected directly 2 brain
- each cranial nerve sends signals 2 brain (e.g. info that’s been computed thru sense organs)
- all cranial nerves part of PNS, save cranial nerve #2 (optic nerve) which is part of CNS
name (+ loosely describe) the 31 pairs of spinal nerves which r connected via spinal cord
note: nerves exit or come in frm above or below vertebrae
1. cervical nerves = nerves C1-C8
2. thoracic nerves = T1-T12
3. lumbar nerves = L1-L5
4. sacral nerves = S1-S5
5. coccygeal nerves (right @ spine base)
how do u get the sensory dermatome (covers entirety of body) frm nerves?
each nerve encodes a diff part of the body
does the dorsal or ventral part of spine receive sensory input
dorsal (which is on back of spine btw)
motor neuron that executes command (output) is situated on which side of spine
ventral side (front of spine)
2 most significant portions of forebrain?
- telencephalon - bulk of outer portion of brain (w folds), most interested in outermost layer (avg. 2.5mm thick)
- diencephalon - has thalamus !
describe telencephalon in Greater detail - what stains can u use 2 look @ it, what do they show/find
- 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 - Golgi stain (only taken up by some cells, but spreads) - shows wiring of cortex/how cells connect 2 each other)
- find: cortex arranged into 6 distinct layers based on cell numbers, arrangement, n connectivity
midbrain ?
connects forebrain + hindbrain
what’s in the hindbrain
- metencephalon
- myelencephalon
what’s the main site of input in a neuron
dendrites duh…
describe axon hillock .
cone-shaped place in junction between soma + axon in neuron
nodes of Ranvier?
situated in gaps between myelin in neuron
what r ‘buttons’ in a neuron
endings of axon branches which release chemicals in2 synapses
what is a neuron’s membrane potential
- separation of charge between inside + outside of cells
- inside of cell kept negative (has approx. -70mV difference compare 2 outside)
what r ions
charged particles w either extra or missing electrons in outer shell
cell membrane structure
channel protein, signal protein, lipid bilayer
what creates resting difference in charge between inside + outside of neuron - v broad view
have pumps in cell’s membrane which set up situation where more sodium is outside (Na+; positively charged)
how many extra electrons does Na+ have
single extra
is potassium (K+) negative or positive
it litch says positive…..
how many electrons is chloride (Cl-) missing
one
what r channels in the neuron context
protein complexes that bridge inside n outside of cells
→ establishment of certain gradients
what’s the concentration gradient like 4 neurons (resting)
concentration highest 4 Na+ outside of cell (wants 2 drift n equilibrate)
what’s the electrical gradient looking like 4 neurons
positive valence (frm outside neuron) attracted 2 inside of cell (negativity)
how is info transmitted w/in a neuron
by transient alterations in the membrane potential produced when ions r allowed 2 cross membrane
when ur looking @ graded potentials, where r u measuring membrane potential frm in the neuron
in dendrite
what r EPSPs
- graded potentials generated @ synapses r EPSPs (excitatory postsynaptic potentials)
- they depolarise cell (make inside more positive, more likely 2 fire action potential)
when ur looking @ APs, where in neuron r u measuring membrane potential frm
axon !
what threshold of intensity is sufficient 2 induce an AP
axon doesn’t respond 2 input until it reaches threshold of intensity (-55mV)
describe summation !
if enough EPSPs arrive @ trigger zone b4 they fade, they can build on each other 2 trigger AP (lasting abt 1ms)
describe the voltage-gated sodium channel
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)
Describe the Hodgin-Huxley cycle
synaptic potential or receptor potential
→ depolarisation of membrane
→ opening of voltage-gated sodium channels
→ sodium going in2 cell
→ further depolarisation etc.
how long do voltage-gated sodium channels stay open
1/2 a ms
when do sodium channels close..
once u get 2 abt +50mV
how does Hodgkin-Huxley cycle end
Na+ (sodium) channels open
→ K+ (potassium) channels open (rising phase)
→ Na+ channels close
→ K+ channels start 2 close (repolarisation)
→ hyperpolarisation
define hyperpolarisation (simple)
membrane potential becomes more negative <3
define repolarisation
K+ leaving cell en masse 2 regain negative charge b4 rebalancing
Na+ K+-ATPase pump - what does it do
maintains the gradient of a higher concentration of Na+ extracellularly + higher level of K+ intracellularly
how do APs move along axon (ignoring myelination) + what r the issues w that
- AP moves along axon thru depolarising enough 2 get each Na+ channel 2 open + then moving on2 next one
- BUT … AP velocity solely thru opening + closing of Na+ channels is only 0.5-2 metres per second (wayy too slow)
ok so how does myelination help w AP conduction velocity
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 !!
myelin sheath def (simple)
mix of fat n protein (insulation like on a wire)
multiple sclerosis is a result of demyelination (when myelin sheath is lost or starts 2 degenerate)… what r the symptoms?
- slow, staggered movement
- impacts on cognition, vision
how long for neural impulse 2 travel frm toe to spine + back
~20 ms
photopic vision. go
cones have this, gives them high acuity colour vision in good lighting
scotopic vision. go
rods have this, it’s poorer acuity achromatic vision in low light levels
why do cones have high visual acuity
bc they have low convergence - single cone signals 2 single bipolar cell 2 single retinal ganglion cell
why do rods have low visual acuity
lots of convergence, pathway goes:
lots of rods
→ less bipolar cells
→ 1 retinal ganglion cell
where r intrinsically photosensitive RG cells (ipRGC) located + why
- mostly located on lower 2/3s of the retina
- 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)
what do the signals of ipRGC do
signals sent 2 the brain govern production of cortisol (day) + melatonin (evening n night)
what photopigment do ipRGC use + where do their axons project 2
- use photopigment melanopsin (this is maximally sensitive 2 blue light)
- axons project 2 the suprachiasmatic nucleus (SCN) instead of image-forming parts of brain
synaptic transmission - what happens !
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
the main excitatory NT in nervous system is glutamate . describe it/what it does
- it’s an amino acid
- 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
main inhibitory NT is GABA . what does it do
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)
in which 3 layers of the eye does depolarisation take place (in a flow-y way)
RGCs, bipolar cells, + photocreceptors r all glutamatergic/releasing glutamate)
which cells in the eye release GABA/ r inhibitory
horizontal + amacrine cells release GABA
→ inhibits synapses 2 their left + right (lateral spread of inhibition)
is lateral inhibition an opponent process (and what is an opponent process)
- yaa
- opponent process is when 2 nervous system processes r Competing
how does simultaneous contrast work (in this example, 2 squares - one has light background, one has dark)
- 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 - darker background:
losing activation bc less light hitting eyeballs, so less lateral inhibition
→ perceived as lighter in colour
what’s another example of lateral inhibition/opponent processes in visual system
Mach bands !
we (humans) can see between 400-700nm wavelengths… what do these signify (ultraviolet etc)
we can see colours between ultraviolet n infrared
what type of wavelengths r more damaging
shorter wavelengths w higher frequency (e.g. gamma ray, x-ray)
what is the opponent-process theory 4 colour perception
colour perception controlled by activity of 2 opponent systems (yellow-blue mechanism, red-green mechanism)
what colour cones r blue cones opposed 2
opposed 2 red + green (yellow)
→ attempts 2 inhibit yellow
→ blue colour after-image when u look @ smth yellow n vice versa
example of opponent processes in motivation
approach-avoidance conflict arises frm competition 2 pursue reward vs. 2 avoid harm
snakes, rats, + mice. what vision type do they have
monochromatic
most mammals have dichromatic vision.. what does this mean
seeing only blues n greens
humans, apes, + old world monkeys - what type vision do we have?
trichromatic - greens, blues, reds
how many photoreceptor types do birds, reptiles, + fish often have
Four
how many colour receptors do mantis shrimp have
12 !! (8 in the visible spectrum, 4 in the UV)
approx. 5-10% of males + 0.1% females r which type of colour blind
red/green
most common type of colour-blindness ..? (1st and 2nd)
- weak in green vision (a.k.a. deuteranomaly)
- no red (protanopia)
how r images projected on2 the retina
images r projected inversely (upside down) on2 retina
when do on-centre, off-surround LGN cells fire
when light is shone right across centre of receptive field (if light shines on periphery, it inhibits activity of the cell)
wld on-centre, off-surround LGN cells fire if light bar was shining in2 centre AND surround
no, no change in firing
r simple V1 cells monocular or binocular
can b either
what does a simple cell in V1 respond 2 best
- elongated bars or edges of objects (Not dots)
- orientation selective (e.g. cld be sensitive 2 diagonal light bars)
- have separate on + off subregions (matters where in visual field bar is presented)
V1 complex cells are..? and have..?
- orientation selective
- nearly all binocular
- have spatially homogeneous receptive fields (no on/off subregions)
columnar architecture of V1. describe this
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
as u go across V1 cortex (instead of deeper), what do u see?
see gradual change in spatial + orientation preference
retinotopy
remapping of retinal image onto cortical surface
which region of the eye uses more of V1
foveal region (greater magnification factor)
retinotopic mapping is an example of What type of organisation
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)
why does V1 use topography (overall + more specifically)
- 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 - facilitates lateral inhibition (if u have inhibitory cells spreading axons laterally 2 inhibit neighbouring cells, want them 2 not have 2 spread too far)
when pressure pulses r close together, is the sound frequency high or low
closer 2gether the pressure pulses r, higher the frequency measured in Hertz (Hz; 1 per second)
pressure pulses travel @ approx. 340 metres per second . T or F?
Trueee
humans can hear 20-20,000 Hz. T or F?
true
how many Hz can chickens hear between
100-2,000
how many Hz can bats hear between
10,000-100,000
how many Hz can dogs hear between
64-44,000
how many Hz can cats hear between
55-77,000
age-related hearing loss - who is most vulnerable + what goes first
- women do a little better w/ hearing thru-out ages
- lose ability 2 pick up on highest frequencies first
2 types of hair cells in ear: inner and outer (describe each briefly)
- inner hair cells transmit mechanical disturbance of membrane in2 electrical signals sent 2 the brain
- 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
transduction def
conversion of sound 2 an equivalent electrical waveform
pathway 2 auditory cortex
cochlea
→ brainstem
→ midbrain (inferior colliculus)
→ medial geniculate nucleus (in thalamus)
→ auditory cortex
describe secondary auditory cortex (A2)
- important 4 sound localisation + analysis of complex sounds
- not necessarily tonotopically organised
why tonotopic organisation in A1?
- saves space + time (like retinotopic)
- 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 - allows u 2 parse out certain frequency bands (scene analysis)
–> e.g. being able 2 clap on beat by dismissing irrelevant frequencies
what is the benefit of beat detection (that tonotopic organisation facilitates)
promotes social cohesion
how else is beat detected/ other frequencies weakened
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
abt 6% of input 2 visual cortex is top-down (most bottom-up). is this statement true?
well yes !
top-down influences on auditory processing
while A1 is larger in macaques than humans,, surrounding areas (belt/A2 + parabelt) in humans r abt 10x larger
–>
so, most connectivity in2 human A1 is actually top-down (around 66% frm other cortical areas)
benefits of top-down influences on auditory processing
- allows context + procedural demands 2 bias perception (esp w similar frequency words)
- better predictive ability
- greater integration of multisensory input
egocentric space def
YOUR relation 2 stuff in space
describe where the dorsal vs. ventral stream r frm V1
dorsal = top of brain, like fin on shark; ventral = straight across
humans have face recognition cells. when can u see/examine them?
when ppl r under surgery….
Quiroga et al. (2005) - what did they find
- found ppl w cells responding 2 Jennifer Aniston - didn’t matter what angle face was presented, cells wld keep firing
- this was the 1st demonstration of face-selective cells in humans!!
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?
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
the Quiroga results display invariance. what does this mean ?
invariance in this context means encoding a representation so that it’s identified regardless of size, orientation etc. (cells respond in same way)
so,,, do we just have special face cells? nothing else?
no!! we have architecturally discriminating cells (e.g. Eiffel Tower cell)
cld cell firing b modulated by familiarity? (study)
- famous ppl don’t trigger that huge a shift in cells, relative 2 someone ur familiar w (e.g. brother, mother)
- BUT cells most triggered when presented w image of some1 recently encountered (e.g. experimenter)
cld the firing of human ‘face’ cells b an emotional response? (study)
presented participants w ‘scary’ things - but didn’t generate cell reaction
‘face’ cells cld b an example of grandmother/gnostic cells . what r grandmother cells?
grandmother/gnostic cells do local coding - so u have 1 highly localised cell 2 represent a given concept
benefits of gma cells/local coding :
assists w discrimination between objects - cells either active during context A or context B
why might the local coding theory not b an accurate explanation 4 ‘face’ cells (key reasons)
- requires huge number of gnostic units (need cell 4 every person u meet, every object u encounter)
- susceptible 2 damage (if ur Jen Aniston cell dies, wouldn’t b able 2 recognise her again)
- generalisation is difficult - how can u solely identify Jen + not just ppl who look like her w/ only one cell?
how many neurons in human brain (how many in hippocampus esp)
86 billion neurons overall, 40 million in hippocampus
the 3 critical goals of visual processing are to:
- separate patterns
- complete patterns - so u have complete mental picture
- generalise - use past info 2 recognise things
dense encoding theory - alternative explanation 4 ‘face’ cells
- don’t have single cell representing item
- 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)
- cells all fire 2gether to give item representation
- there IS some overlap tho,, which is a detractor 2 the theory
what is distributed encoding (beyond it being a mix of local + dense encoding)
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 generate separate representations, while having sufficient overlap 2 get generalisation + pattern completion
what is principal component analysis
simplifies large amounts of data while maintaining important trends etc.
what did Doris Tsao do (finding evidence 4 distributed facial representation code)
- identified 50 dimensions that varied most across faces (25 for shape, 25 for appearance)
- manipulated images 2 get new faces along any of these 50 diff dimensions (e.g. might change shading)
- recorded cell activity in the middle lateral, middle fundus, + anterior medial ‘face patches’ when participants presented w images on screen
what did Tsao find
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 !!
what’s important abt Donald Hebb (1904-1985) . speak Broadly
- thought abt how a series of interconnected cells could possibly store info
- heavily influenced fields of neurosci, computational science
in order 2 prove LTP is a mechanism 4 learning, u need to show..:
- show that blocking LTP prevents memory formation
- show that reversal of LTP produces forgetting
- show that learning leads 2 LTP-like changes
- show that producing LTP creates false memories or masks existing memories (v difficult/impossible 2 do)
LTP requires activation of NMDA subtype of glutamate receptor . T or F?
true duh
AP5/APV selectively block NMDA receptor. T or F..?
True
LTP maintenance can be prevented by the drug ZIP (zeta-inhibitory peptide). T or F?
True
V1 is for orientation (largely), V4 is for colour perception, + V5/MT is 4 motion detection . T or F?
true
Patient M.P. had bilateral lesions of V5. T or F?
True
how was patient M.P. impaired
motion perception was drastically impaired (saw things like slowed-down frames), while colour perception etc. remained fine
all cells in V5 have direction tuning ..what does this mean?
only fire when stimuli move in a certain direction
V5 cells r also tuned 2 things moving @ specific speeds . T or F?
T
optic flow def
looks like whole world is moving as u move thru it
looming def
detection of change in visual angle as you approach an object (object expands + becomes bigger)
what is the binding problem
challenge of preventing the properties of one object representation frm being mistakenly assigned 2 another
temporal binding (possible solution 4 how brain recognises features of one object as belonging 2 That object): how does it work?
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
what was Karl Lashley (psychologist)’s theory of the biological seat of memory, and how did he get there (hint: rats and Maze)
- 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 - 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)
in 1953, H.M. Trashed Lashley’s theory. yes or no?
yess
describe H.M.’s case (also,, Scoville was his surgeon) - how did he disprove Lashley’s theory
- 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) - 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
semantic memory def
facts
episodic memory
memory of (life) events
p.s. H.M. had severe amnesia 4 episodic memories, while semantic memory was less affected
disrupting the hippocampal circuit: patient R.B.
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
ischemic event def
loss of blood supply - heart attack or stroke
Rey-Osterrieth figure test
get presented w image + asked to copy it (first when it remains in front of subject, then after it’s been taken away)
rhinal cortex def
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. ….
diencephalic amnesia characterised by..?
deficits in anterograde memory (?) + retrograde amnesia, w preserved motor learning
patient N.A. - what’s their story ?
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)
Wernicke-Korsakoff Syndrome or ‘wet brain’ or ‘Beriberi’
- 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 - amnesia due 2 heavy drinking basically …
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
- everyone w temporal lobe damage performs vv poorly
- alcoholics might have reduced performance compared 2 non-alcoholic controls
specific episodic memory task (how many items frm a story can u repeat back): how do alcoholics perform?
ppl w alcoholism perform slightly worse than non-alcoholics, but still wayy better than ppl w temporal lobe damage
where does binding of info occur 2 create one whole memory
in input stages frm cortex 2 hippocampus
overview of hippocampal diencephalic memory system
- info comes frm cortex
→ hippocampus
→ white matter tract (fornix to mammillaries)
→ anterior portion of thalamus
→ info gets further consolidated in neocortex - awlso,, amygdala receives hippocampal input → projects 2 hypothalamus
what shld damage 2 the hippocampal diencephalic memory circuit produce ?
- deficits like in H.M.
- BUT remote memories (1-2 years+) don’t depend on this circuit in the same way
why don’t 1-2 yrs+ memories depend as much on the hippocampal diencephalic memory circuit
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
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
yes, he would’ve
what encodes the ‘where’ aspect of episodic memory
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)
allocentric reference def
looking @ where everything else is
- e.g. using east or west to locate people (external world)
water maze results (variable start/allocentric point of reference)
rats w lesioned hippocampi Can’t learn → hippocampus v important 4 allocentric representations of space
water maze results (egocentric point of reference - starting in same place each time)
rats w lesioned hippocampi took longer 2 learn than controls
→ after 12 trials, performance is abt the same
takes 4 yrs of training 2 learn London’s 25k streets . T or F
true
cabby driver vs. control (hippocampus volume)
increased posterior hippocampal volume in taxi drivers compared 2 controls,, decrease in anterior portion
comparing hippocampi of taxi vs bus drivers
- increased posterior volume in cabbies only
- taxi drivers performed worse on Rey-Osterrieth complex figure test
receptive field of hippocampal place cells? what do these place cells do
- 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 - 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
chronoception
study of time perception (subjective experience of time)
time production experiment (THC)
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
time estimation experiment (THC)
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
SCAD (suspended catch air device) study - go 2 v high platform, fall + r caught by net → time seems to slow . detail this further
b4 participating in fall, estimated fall duration not that much (2s)
–>
after participating in fall, estimated fall duration seems much longer (3s)
chronostasis def + example in vision
- halting of time
- 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)
flash lag illusion explained
neither red or blue square is larger, NS is locating the squares forwards in time (i.e. where they Will be in the future)
Scalar Expectancy Theory (SET) model of timing
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
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
4.5 second estimation
what cld pacemaker b in brain?
- 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 - ramping up
→ as u get closer in time 2 goal (e.g. getting gift), cld have a broadening in neuron firing rate
hippocampal time cells (found decade ago) r capable of what..? + also what is evidence 4 them existing
- representing passage of time
- 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)
humans normally good @ estimating period of time of up to at least 20s . T or F
T
interval reproduction study (asked H.M. + control group 2 estimate amt of time that command took) … results?
- control good @ estimation, H.M. Not
- as u increase period of true time, trend continues w H.M. perceiving more time than there was
see other ppl w temporal lobe amnesia also having time perception issues (Buzsaki & Llinas, 2017)
- took controls + ppl w temporal lobe amnesia on tour of their facility
- @ each time point, certain things happened (e.g. someone dropping smth on the floor)
- asked to regurgitate memory of whole tour
- ppl w temporal lobe amnesia reported fewer episodes AND their sequence of events was completely jumbled up
valence def
positive or negative emotional value ascribed 2 memories
Memory for 9/11 study
- had 2 groups - downtown (close to site) + midtown (farther away)
- asked them 3 yrs after event 2 report their memory of that day
- downtown group had strong memory of 9/11,, midtown not sm
→ closer u were 2 twin towers, stronger ur recall of that day - also asked 2 recall memories of previous summer
→ way better recall 4 9/11 than previous summer 4 downtown group
lecture material is better remembered after post-lecture arousal. evidence?
- given mini test 2 weeks after lectures finished
- lectures days 1 + 3 identical, day 2 they showed groups 2 diff videos (control given boring video, experimental given graphic clip of oral surgery)
- students shown graphic video had better recall of day 2 lecture than controls
CNS stimulants can enhance memory if timing is right. evidence?
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)
where r adrenaline/epinephrine + cortisol produced
adrenal gland
adrenaline is both a hormone + NT (difference is target organs) .. elaborate a bit
- hormones released by gland somewhere in endocrine system shld b acting on diff organ system
- NTs shld b acting specifically on neural cell types
where is adrenaline released + what controls its release
- adrenaline released by adrenal medulla (inner portion of the adrenal gland) which regulates + secretes adrenaline in response 2 stress
- release is controlled by the hypothalamic-pituitary-adrenal (HPA) axis
can adrenaline cross BBB
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
vagus nerve def
- nerve that runs frm brainstem to peripheral organs
- sends + receives signals frm organs
When is cortisol known as when used as medication
Hydrocortisone
Can cortisol cross BBB easily
Yes
what is cortisol, what processes is it involved in
- steroid hormone, initially formed frm cholesterol
- involved in processes including metabolism + immune response
cortisol is released by HPA axis. describe this more
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
amygdala activity during film viewing correlates with recall 3 weeks later . give more details
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)
slow cortisol release doesn’t seem beneficial 4 memory … how does the Yerkes-Dodson Law come in here
well: lil bit of stress good 4 u (thru adrenaline route),, but ongoing stress damages ability 2 retain memory (cortisol route)
Do both quick (adrenaline) + slow (cortisol) ways that stress hormones act activate the amygdala
Yes, which in turn activates hippocampus
Alzheimer’s disease most common form of dementia. give a brief definition of dementia
when a person experiences gradual loss of brain function due 2 physical changes in brain
what causes dementia
- Alzheimer’s
- vascular dementia (e.g. after stroke, loss of neurons in damaged area)
- Lewy body dementia (build up of proteins in2 masses known as Lewy bodies)
- frontotemporal dementia (degradation in frontal + temporal lobes)
stressor effects on memory are mediated by the amygdala (rat study) …
- had controls + rats injected w amphetamine in the amygdala (amphetamine boosts amygdala activity)
- two conditions 4 amphetamines:
one group immediately injected, other is 2hrs after final training trial - only rats given immediate amphetamine injection much quicker 2 find platform
–>
soo boosting activity of amygdala soon after learning smth boosts retention of memory
what is the prognosis 4 Alzheimer’s
6-10 yrs
describe what tests u can do 4 Alzheimer’s … phonemic + semantic verbal fluency (SVF)….
- phonemic fluency - tell me as many words as u can in 1 min starting w letter ‘b’
- semantic fluency - tell me as many animals as u can in 1 min
measure no. of correct words
prevalence of Alzheimer’s by age group
- up until 60, 1-2% of global pop.
- once ur 65, likelihood of developing condition doubles every 5 years
- @ 85 have approx. 20% prevalence (NZ)
how many cases of Alzheimer’s rn
approx. 50 million
–> on course 2 overtake stroke + heart attack economic burden combined
brain changes in Alzheimer’s
- extreme shrinkage of cerebral cortex
- extreme shrinkage of hippocampus
- severely enlarged ventricles
- 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
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
by 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
list some cholinesterase inhibitors
Donepezil (Aricept)
Rivastigmine (Exelon)
Reminyl (Galantamine)
what r some Horrors (biologically) that r associated/may cause Alzheimer’s
- plaques - aggregates of protein beta-amyloid, clump 2gether outside of cells (impair synaptic function)
- neurofibrillary tangles - aggregates of tau protein (clumps of proteins that group 2gether inside cell)
Amyloid precursor protein (APP) is a protein w an important role in synaptic plasticity. T or F?
true
how is beta-amyloid produced (bearing in mind over-production of beta-amyloid is associated w Alzheimer’s)
beta-secretase + gamma-secretase cleave APP protein → beta amyloid produced
what prevents beta-amyloid formation
prevented by alpha secretase cleaving APP protein
Aducanumab - antibody against beta-amyloid formation (monoclonal antibody) . was/is it useful 4 AD
no !
does beta-amyloid plaque location map on2 symptoms well..?
no,, some ppl have lots of beta-amyloid plaques w no AD symptoms
why was study on beta-amyloid oligomer AB*56 published in Nature (2006) fraudulent
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)
western blotting def
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
what does Donanemab (antibody, came out in 2023) do
- radio-labelled amyloid plaques across 76 weeks (people either given antibody or placebo)
→
plaques broken down by antibody Donanemab - cognitive decline was slowed by approx. 35% over 18 months
in a healthy neuron, there’s a scaffold (cytoskeleton) that the cell is built around . how does tau protein relate 2 this
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)
in AD, tau proteins leave the microtubules … what happens next?
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
tau protein buildup maps onto AD symptoms wayy better than beta amyloid . T or F?
true
Braak stages (Tau protein)
- tau protein 1st starts 2 show signs of aggregating in medial temporal lobe (start off in transentorhinal region)
- tangles spreading thru entorhinal cortex + starting 2 b visible in hippocampus
- get lots more tau deposition, not just in entorhinal cortex + hippocampus but in other areas of cortex too
what r ur chances of developing early-onset AD if one of ur parents has it + what mutations is it linked 2
- 50%
- mutation on PSEN1, PSEN2, APP genes
early-onset AD (present @ less than 65 yrs; mostly familial, not necessarily genetic) makes up what percentage of total AD cases
5%
what do astrocytes do (that’s relevant here)
take stuff frm blood supply + put on2 neuron 2 provide metabolic support
late-onset AD (sporadic, 95% of cases) … what is risk related 2
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
what does APOE gene do
produces protein mainly found in astrocytes
→ protein transports cholesterol frm astrocytes 2 neurons
how is APOE4 integral 2 BBB… start off by describing BBB
- 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 - APOE4 can disrupt formation of tight junctions, opening up BBB (making it leaky)
→
selectively impairs function of pericytes
what r endothelial cells
blood capillaries
why does BBB exist
2 keep blood separate frm brain tissue (blod is toxic, has lots of iron)
study looking @ people w APOE4 + their cognitive decline, level of pericyte injury… what were the results
gave ppl mental state exams @ 2 year intervals
–> rate of cognitive decline much steeper 4 individuals w higher levels of pericyte injury
University of Minnesota ‘Nun Study’ (what might protect against AD): method
- 678 nun participants
- wrote early life autobiography @ average age 22
- 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)
University of Minnesota ‘Nun Study’ (what might protect against AD): findings
ppl w high density scores early in life (detailed accounts) associated w intact cognition later on, regardless of AD lesions
what percentage of dementia cases worldwide are preventable
45%
name the bits of our prefrontal cortex
- dorsolateral prefrontal cortex
- ventrolateral prefrontal cortex
- orbitofrontal cortex
- medial prefrontal cortex (inner part of prefrontal cortex)
- anterior cingulate cortex (ACC)
lateral = out to the side; ventro = lower .
T or F?
true
what damage did Phineas Gage incur age 25
rod went thru skull, damaging ventromedial region of both frontal lobes + sparing dorsolateral
classic working memory test/delayed response task
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
what does PFC cell firing look like during delayed response task
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
prefrontal lesions impair working memory performance (study)
- groups: VM damage, right DL/M damage, left DL/M damage
- for all, decreased performance in 60s
- all of prefrontal lesioned individuals had worse working memory performance compared 2 controls (esp right DL/M prefrontal cortex)
n-back test (4 working memory)… describe
- 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)
- 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)
n-back test findings (PFC, lures)
- increased activity in PFC (dorsolateral) during task, esp when lures r presented
- working memory span associated w ability 2 suppress non-relevant info (lures)
Tower of London test outline + what does brain-scanning during task show
- have initial configuration + target configuration (have to turn into target configuration in least number of moves)
- activation in PFC (esp in dorsolateral PFC, a.k.a. Brodmann Area 46)
why is the PFC involved in working memory?
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)
inhibitory (self-) control def
where previously reinforced, highly reinforcing, or well-learned (habitual) responses have 2 b suppressed
successful self-regulation associated w top-down control frm the PFC over subcortical regions involved in reward + threat processing . T or F?
true
hot/cool framework
- hot system
- emotional, reflexive
- develops early in childhood, accentuated by stress
- might b some sort of stimulus which provokes that reaction - cool system
- using past experience 2 decide behaviour
- comes on later in brain development, requires self-control
utilisation behaviour (+ environmental dependency): guy w damaged PFC (studied by Lhermitte, 1983)
experimenter takes off glasses
→ patient sees them, picks them up, + puts them on his own head
→ utilisation behaviour (driven by a certain sensory stimulus)
test of frontal lobe function: Wisconsin card sorting task
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)
Performance in a go/no go task (impulsivity): method
- Followed ppl up 40 yrs after Mischel’s marshmallow task (divided in2 low + high delayers)
- Shown faces, told 2 sort by sex
- Cool task = neutral faces; hot task = emotional faces
Performance in a go/no go task (impulsivity): results
- false alarm rate higher 4 low delayers
→
delayed gratification @ 4 yrs old indicative of impulsivity later in life - 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
self-control (Dunedin Study)
- self-control assessed between age 3-11, adult outcomes assessed at 32
- have childhood self-control scores plotted against adult criminal conviction
- low (score of 1) childhood self-control associated w an approx. 45% chance of having criminal conviction by 32
how does effortful training work + does it boost self-control
- specific focus on attention + working memory
- usefulness: seems 2 b selective to task, limited generalisation
How does effortless training work + does it boost self-control
- Mindfulness, flow states, nature exposure
- Useful ! works !!
set shifting (changing strategy ur using): trail-making test
- Part A: asked to move from diff positions, then join up dots
- Part B: go again in sequence, but alternating between numbers + letters
- score correlates w dorsal PFC thickness
why is dorsolateral PFC so involved?
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
concrete thinking
reasoning that’s based on present experience
name some ways 2 test 4 abstract thought
- Raven’s Progressive Matrices
- delayed match-to-sampling task
- proverb interpretation
describe Raven’s Progressive Matrices (test of non-verbal reasoning, abstract thought)
- stages: matching, figural, analytical (requires most abstraction)
- brain activity during task: during analytical stage there’s lots of DLPFC activity
→ abstraction cld b dependent on DLPFC
delayed match-to-sampling task: looking @ the neurons in monkey DLPFC
- implanted electrodes in DLPFC, paired presentation of sample w particular cue (e.g. certain tone)
- e.g. of idea: if u hear certain tone, need 2 obey non-match rule; if certain tone not present, obey match rule
- results: DLPFC fired regardless of what rule was 2 b followed → cld point 2 existence of general rule cells ?
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
for the proverb ‘Rome wasn’t built in a day’, a concrete error might be ‘Rome is a beautiful city’
what’s the proposed anterior-posterior organisation of PFC
further anterior (front) u go, more cells u get w abstract thought
action hierarchy
all the things u need in place to achieve ultimate goal
cognitive control during planning + execution involves:
- identifying primary + subgoals
- retrieval + selection of relevant info
- simultaneously maintaining multiple subgoals
- determining what’s required 2 achieve goals
- anticipating consequences
vmPFC lesions + ability 2 organise behaviour: multiple errands study
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)
prefrontal lesions + the ability 2 organise behaviour: multiple errands test
- looked @ individuals w frontal lobe damage
- gave them 8 tasks, 6 of which were simple
- 7th required some future planning, 8th difficult
- individuals w frontal damage couldn’t plan v well, got confused
→
overall less economical way of completing tasks
sculpting the response space def
role of DLPFC 2 define a set of responses suitable 4 a particular task n then bias these 4 selection
study where u make the following problems true by moving 1 stick … (what r the results 4 ppl w lateral PFC damage)
- 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 - 1st problem easy, both do well; 2nd hard, ppl w lateral PFC do worse
with PFC damage, looking more @ ppl’s deficits than a sudden greater creative ability… provide an example
e.g. lack of inhibition (can’t stop drawing; perseveration)
most patients w FTD have decrease in divergent thinking (which is integral 2 creativity). T or F?
true
creativity-related performance: controls, patients w bvFTD (behavioural/frontal variant), + semantic/temporal dementia (SD)
from best 2 worse scores in creativity: controls → bvFTD → SD
→ ppl w frontal lobe damage not more creative
Symptoms of frontal lobe syndrome
- Cognitive impairments (deficits in temporal ordering, poor decision-making → dysexecutive syndrome, etc.)
- Emotional changes (apathy, anergia, etc.)
- Behavioural deficits (utilisation behaviour, perseveration, environmental dependency, etc.)
anergia def
lack of energy
Balint syndrome causes + def
- Typically a bilateral lesion of the parietal lobe
- Can only perceive one object @ a time
what damage is visuospatial neglect associated w
right parietal lesions
signal detection task:
when u attend 2 stimulus + correctly perceive it being there (get hit), this is correlated to activity in …?
right lateral PFC
signal detection task:
decision 2 act involves activation of… ?
medial PFC
signal detection task:
what part of the PFC is involved when ur biased (e.g. 2 respond ‘yes’)
bias impacted when left lateral PFC damaged
PFC damage (mostly) associated w decreased performance in tasks w creative elements (such as originality, flexibility, fluency). T to F?
true
what is the primary gatekeeper 2 working memory
attention
frontal cortex provides important top-down control by directing attention. T or F?
true
dual systems model of decision making. describe
- system 1 (experiential-affective): quick, mainly based on emotions @ the time
- system 2 (analytic): rational, rule-based → slower, it’s conscious + not automatic
system 2: delay/temporal discounting (study - lesioned orbitofrontal cortex)
- $20 now or $12 six months down the line
- most wld take $10 → discount value based on the amt of time it takes 2 get
- ppl w lesioned orbitofrontal cortex tend 2 discount value much sooner (patience runs out after 2 wks)
system 2: how long shld animal stay in a particular spot foraging b4 moving on (getting diminishing returns as u exploit piece of land)…. exploit/explore trade-off !
marginal value theorem: strategy where u move on once the instantaneous energy intake frm the patch is equal 2 the habitat average
how r anterior cingulate cortex neurons related 2 patch-leaving (system 2)
longer u spend time exploiting patch,, more these neurons increase their firing rate
→
when firing rate is more or less doubled, that’s when u move on
damage 2 the anterior temporal lobes (including amygdala) produces the Kluver-Bucy syndrome . what r the symptoms of this
- get hyperphagia (over-eating)
- hypersexuality
- hyper-orality (investigating things w mouth)
- placidity/docility/lack of fear
study (amygdala): looked @ ppl in ground zero of 9/11 (w/ in 2.5km of twin towers) + control group frm far away
- 3 yrs after event, using MRIs
- presented calm or fearful face, had 2 press ‘go’ button →
9/11 exposed showed much greater amygdala activation when shown fearful face
why is amygdala involved in fear response ?
emotional processing in amygdala is projected 2 the ventromedial PFC + anterior cingulate cortex
vmPFC involvement in emotional processing ….? examples
- Phineas Gage had vmPFC lesion,, was fitful, cared Nawt for restraints that conflicted w his desires
- when recalling or anticipating pleasant events, vmPFC is activated
Damasio’s Somatic Marker Hypothesis (SMH) def .. and how does vmPFC relate 2 this
- if there’s any ambiguity, turn to body’s state/feelings 2 make a decision
- vmPFC (esp orbitofrontal) critical 4 triggering somatic changes in response 2 stimuli such as cues 4 reward or punishment
→ might alter decisions
Galvanic Skin Response (GSR; vmPFC)
- put electrodes on palms of hands, give them stimuli
- measure fluctuations in GSR 2 get some read of their emotional state
- ppl w vmPFC damage failed 2 show autonomic emotional responses 2 arousing stimuli (innate responses such as 2 a loud noise were still intact)
Iowa Gambling Task basic overview
- have 2 decks,, deck a: high risk, high reward, long-term loss; deck b: low risk, long-term gain
- tell ppl they have 2 keep turning cards over until they choose which deck is most advantageous
- skin conductance response (SCR) measured frm palms
Iowa Gambling Task: amygdala or vmPFC damage.. results?
- controls made more selections frm deck B (good deck), while subjects w either type of damage never showed that bias
- anticipatory (b4 turning over card) SCR: controls had greater SCR generally, but esp when they were abt 2 turn over card frm ‘bad’ deck
- reward + punishment SCR (after you’ve turned card over): controls had greatest SCR when they chose frm bad deck + got bad card, response blunted completely 4 individuals w amygdala damage, + ppl w vmPFC damage Did have response (capable of emotion)
does discrimination occur prior 2 conscious awareness? (Iowa Gambling Task)
anticipatory SCR level tends 2 taper off w good deck, but stay high w bad deck
→ stop selecting frm bad deck, start selecting more frm good deck
→ so,,, type 1 emotional system Can feed in2 later conscious decision-making (conceptual stage)
why is the vmPFC So connected w emotional response and memory?
bc it connects bidirectionally w the amygdala + hippocampus
the gradient frm ‘hot’ to ‘cold’ system is medial PFC to lateral PFC. T or F?
true
alcohol consumption inhibits PFC activity.. what is a study that looks @ this/what exactly did they find
- participants were under one of 3 conditions of alc consumption: placebo, moderate, high
- given a go/no go test
- found: less activation of PFC w more alc
PFC activity inhibited w threat/fear .. what study shows this/what exactly did they find
- participants anticipating toe tap,, have 2 tap button w/ in 240ms to avoid it
- trial lasts 15s
- vmPFC more active in stage 1 (when threat is lower)
→
supports hypothesis that vmPFC activity is inhibited w threat/fear
study looking @ ppl waiting for dentist appointment vs. comedy show (describe)
- have 2 buttons, one will give higher reward + one will give a loss
→
have to make decision abt which one gives reward - fearful group tended 2 sample more (press buttons more) b4 choosing, but were less likely to switch between buttons
→ PFC activity inhibited by fear..
how many languages in PNG
700+
when do children start babbling
@ 7 months
when do children generally have their first words
by a year
when r children making short sentences
by age 2
language is lateralised 4 right-handed ppl (largely in the left hemisphere, left temporal cortex). T or F?
true
how is language lateralised 4 left-handed people?
65-70% language lateralised 2 right hemisphere, remaining ones have either left or no lateralisation
what r the two main arteries feeding the brain + what projection do they follow
- carotid + vertebral (bilateral, have them on both sides)
- they follow an ipsilateral projection
what does a Wada test test for.. and how
- tests 4 lateralisation
- you inject anaesthetic in2 one side of the carotid artery,, then get preferential spread of anaesthetic (+ dye) 2 one (active) hemisphere
what is a reason why surgery might b done 2 split the corpus callosum in half
so that seizure generation can’t spread frm one hemisphere 2 another ! (prevents transmission of info)
split-brain patients reported items flashed in RVF + denied seeing LVF stimuli . why?
- LVF info feeds in2 right hemisphere, which is not in control of language (can’t articulate that they’ve seen the stimuli)
→
generative syntax only exists in one hemisphere (left) - important 2 note that LVF info can produce behaviour (e.g. left hand can correctly retrieve objects presented in LVF), despite not being able 2 produce speech
define ‘prosody’ simply + what hemisphere it is associated w
- stress that u place on certain words- pitch, pauses, loudness
- believed 2 involve areas of right hemisphere
study looking @ the effect of lesions 2 right hemisphere (superior temporal gyrus) found..?
- say certain words + identify associated emotion
- individuals w STG damage have difficulty picking up on emotion thru language
how wld u explain lexical selection (simple)?
what word is the best match??
describe the Wernicke-Lichtheim model
- auditory input
→ Wernicke’s area
→ get 2 other area holding conceptual representations → enable Broca’s area (premotor area)
→ motor output (speech) - direct link between Broca’s + Wernicke’s areas thru the arcuate fasciculus
aphasia is observed in what percentage of strokes?
40%
what is an ischemic stroke
might have blockage 2 blood vessels depriving brain regions of blood
what is a hemorrhagic stroke
blood gets in contact w brain tissue
what is a transient ischemic attack/TIA
- known as a ‘mini stroke’
- usually around 5 min blockage, not always damaging but higher risk of having full stroke w/ in a yr
pure word deafness simple def
might not b able 2 perceive spoken word
Wernicke’s/fluent aphasia involves ..?
issues w word comprehension - words have been strung 2gether either incorrectly or out of context
what does transcortical sensory aphasia involve
impaired comprehension, intact repetition
transcortical motor aphasia def
difficulty finding words, intact repetition (Broca’s area intact)
conduction aphasia (damages arcuate fasciculus) has what symptoms/traits
deficits in repetition !
anomia
inability 2 name objects, incorrectly naming objects that ur perceiving
agrammatic aphasia
misunderstanding of complex sentences
apraxia def
difficulty in the sequencing of articulations
dysarthria def
issues controlling speech muscles (weakness, slowness, slurred speech)
Warrington and Shallice study … what did they find
looked @ ppl w left-hemisphere lesions
–>
found they had category-specific mnemonic deficits
semantic somatotopy def
if ur thinking of/hear word, you’ll get activation in parts of motor cortex it corresponds 2
→
fits w understanding of hippocampal-diencephalic memory system
semantic dementia def
- caused by frontal-temporal degeneration, first affects language areas of the temporal lobe
- results in general loss of conceptual knowledge
hub and spoke model- what is it?
basically all projections r connected 2 temporal cortical area (hub),, w diff brain regions as ‘spokes’ processing particular info b4 feeding it back 2 the hub
–>
this creates overall conceptual representation
When ur reading, you’re trying 2 create situations that tell us abt the meaning of words (situation models).. Stanfield & Zwaan (2001) looked @ ‘nail’ in a situation model. What did they find?
- Participants given sentences: ‘he hammered nail in2 wall’ or ‘hammered nail in2 floor’
- Presented w image + asked if it fit w the sentence (yes or no)
→ if nail’s orientation in image matched w story (e.g. nail was horizontal if ‘wall’ was the sentence presented), RT was faster
Where do u get brain activity when using situation models
- Inferior parietal cortex
- Posterior cingulate cortex
- Precuneus
- Medial PFC
- Anterior cingulate cortex
- Parts of medial temporal lobe
Bransford & Johnson (1972) presented participants w winding paragraph (untitled vs. titled).. what did they find
- higher comprehensibility rating when titled
- fMRI results: get activity in more brain regions (particularly in left hemisphere) when titled
what r the 4 main dimensions of social behaviour (Wu & Hong, 2022)
affiliative, antagonistic, self-benefitting, other-benefitting
key processes that underpin social interaction are..? (Molapour et al., 2021)
- social perception
- social inferences (e.g. mentalizing - ability 2 understand the mental state that underlies behaviour)
- social learning
- social signalling
- social drives - bonding, social reward, social status
- social identity - can infer smth abt someones identity just by looking @ them (inferring someones age, status)
premotor cortex (area F5c) involved w social cognition.. how exactly?
- mirror neurons found in ventral premotor cortex
- mirror neurons fire when u see someone carrying out the same behaviour u do (fire both when ur carrying out behaviour + observing it)
simulation theory def
proposes that part of our ability 2 understand others is based on our ability 2 mimic their experience (2 mentalize and empathise)
–>
mirror neurons therefore Very important 4 whanaungatanga
what r the response properties of a mirror neuron (Casile et al., 2011)
big spike in cell firing when monkey performs motor response
→ same cells also fire when watching someone else perform same task
mirror neurons r also found in inferior parietal lobule (PFG) + superior temporal sulcus (mirror neurons here only fire when animal is observing)… T or F?
true, duh
study looking @ TMS applied 2 either hand or lip area of premotor cortex (deactivating these areas; Michael et al., 2014)… what did they find
- presented context slides (e.g. house), then image of hand or lip
- participants then 2 select most appropriate tool frm image displayed (e.g. radio or hammer)
- if the appropriate tool was associated w the lip + TMS inhibited lip premotor area,, participants had worse performance (hit rate/correct responses wld go down)
→
supports idea that mirror neuron activity allows u 2 put urself in the position of what ur seeing (important 4 empathy)
what was the set up 4 Gallo et al. (2018)’s study on brain areas involved w generating empathy
- participants led 2 believe confederates were being harmed,, cld donate their own earnings (frm the study) 2 reduce impact of punishment
- had 2 levels: face (not seeing strike, just confederate facial expression), slap (seeing strike)
what is the somatosensory cortex involved in
involved in empathy 4 actually Feeling someone else’s pain
what did Gallo et al. (2018) find ?
- as u go up in intensity of strike in both conditions, ppl become more willing 2 donate
- when TMS applied over primary somatosensory cortex (inhibiting activity)
→
not much change in face condition but in slap condition there is a reduction in empathy slope (bc ur less capable of mirroring what ur seeing)
vmPFC is associated w which system?
‘hot’, emotional one
Lee et al. (2010) looked @ how medial frontal damage affected performance on Faux Pas Test.. what did they find?
Participants w medial frontal damage had difficulty w questions where u had 2 understand others’ mental states
briefly describe the Faux Pas Test
- read paragraph out 2 someone + see if they can spot the faux pas and show understanding of why it was a faux pas
- elements of the test:
> detecting faux pas
> understanding faux pas
> understanding recipient’s mental state
> understanding speaker’s mental state
> details of story (control question)
what r the core components of social connection according 2 Holt-Lunstad (2018) .
- structural
- functional
- quality - the positive + negative aspects of social relationships (e.g. might belong to group but not in a good way)
what impact might social factors have on mortality (looking @ percentage of women surviving over 18 years; Pantell et al., 2013)
- age-matched groups, asked 2 score their social network (low score = most perceived social isolation)
- found: dose-dependent effect of social isolation on mortality (higher the perceived social isolation, higher the mortality)
percentage of individuals developing dementia over a 3 year period (Holwerda et al., 2014).. what did they find (looking @ social connections, loneliness)
- living w others (6%)
- living alone (9%)
- not feeling lonely (6%)
- feeling lonely (13%)
social control hypothesis (why does social isolation matter)
whānau may impact positively on health behaviours thru obligations etc. (diet, exercise)
briefly outline the evolutionary hypothesis (why social isolation matters)
- isolation can b dangerous (e.g. can’t fight off lion by urself)
→ evolved 2 make isolation feel uncomfortable - also evolved 2 make isolation activate brain regions promoting short-term preservation (e.g. increased vigilance, anxiety)
marital status + cortisol levels (Chin et al., 2017).. findings?
those who r currently married have lower cortisol levels than those never married or divorced
–> supports evolutionary hypothesis
11 year follow-up of dementia-free individuals originally aged 60-70 (Ennis et al., 2017).. what did they find
those w higher cortisol levels more likely 2 develop Alzheimer’s later on
survey of 20k U.S. adults (regarding loneliness etc.) found that..?
- 40% felt alone
- 47% felt left out
- 27% felt misunderstood
- 43% felt that their relationships were not meaningful
- 43% felt isolated
does connection thru the internet substitute 4 face-to-face interactions? (Primack et al., 2017)
- 1800 U.S. adults, social media use on 11 platforms
- self-reported measures of perceived social isolation
- found: ppl w highest quartile of social media use had twice the odds of perceived social isolation than those in lowest quartile
two important aspects of consciousness:
- wakefulness
- awareness of the enviro + self
according 2 Herculano-Houzel (2009), what animals (including humans) have more neurons in cerebral cortex
humans have more neurons in cerebral cortex, primates a bit behind, then rodents, then insectivores, then ants
mirror self-recognition (MSR) as a test of self-awareness
- put dot of paint on infant’s nose, eventually infant will figure out that image in the mirror is them
–> realise that they must have a dot on their nose, pass the test by touching mark on themselves - apparent self-recognition in ants + elephants
issues w the MSR test as measure of self-awareness
cld b matching kinaesthetic sensation to visual perception
–> know you can make image move, even if u don’t know image is you
what types of memory come under conscious memory
explicit/declarative → episodic, semantic
looking @ consciousness in Rhesus monkeys (Hampton, 2001)
- monkeys given choice between memory task (cld get good reward) or not doing task and getting worse food pellet
- monkeys more accurate when they choose 2 take test instead of being forced
–> choice 2 take test influenced by their awareness of their own memory - as delay after stimuli presentation increases, monkeys less likely 2 choose 2 do task (less sure of memory)
–> indicates they have some level of consciousness
what r the neural correlates of consciousness (NCC)?
the smallest set of neural processes necessary 4 consciousness sufficient for a given conscious percept or explicit memory
what does the reticular formation (strip of nuclei running length of the brainstem) do
it has cells that project + release arousal NTs (e.g. norepinephrine)
–> gives u waking experience/consciousness
briefly define ‘minimally conscious state’ + the underlying brain activity or damage
- characterised by fixation, response 2 simple commands
- reduced cortical activity
briefly define unresponsive wakefulness syndrome + its aetiology
- characterised by open eyes, but it’s just reflexive behaviour
- caused by damage 2 cortex and/or thalamus
locked-in syndrome (fully conscious but unable to move) is caused by..?
- damage 2 ventral part of pons (No cortical damage)
- as many as 35% of non-responsive people might have syndrome
what is bistable perception
observer perceives the same stimuli in 2 different ways (e.g. of a bistable percept wld be Necker cube)
using binocular rivalry (bistable task) 2 look 4 brain regions involved in consciousness .. how does that work
- have goggles over eyes, diff image shown 2 each eye
- one image dominates, then after a while other image takes over
- rivalry demonstrates that ur having conscious experience since stimulus is fixed
→ can measure brain activity changes during task 2 localise consciousness
which brain regions did contrast studies (using a brain scanner) identify as responsible 4 conscious perception
found a network of parietal + occipital areas showing activity changes (Not in v1)
> extrastriate occipital lobe regions involved
what is propofol-induced anaesthesia + what r its implications 4 alcohol consciousness
when u give someone propofol-induced anaesthesia, see decreases in long-range connectivity + localised decreases in synchronous firing
→
can imagine some diminished connectivity w drunkenness (less conscious experience)
brain activity during lucid vs. non-lucid REM sleep (fMRI)
- parietal, temporal, + prefrontal cortex all more active during lucid REM sleep
- lucid dreaming also associated w greater functional connectivity between/in those regions
can apply TMS over cortex when ppl r waking or sleep 2 determine consciousness .. how?
- if applied while awake, EEG recording will show complex wave; in early stages of sleep = less complex wave; deep sleep = even less complex wave
- see much greater spread thru-out cortex when ppl r awake (functional connections more active while awake)
→
can see a breakdown of functional connectivity during non-REM sleep
→
therefore, impairment in ability 2 integrate info frm diff brain regions is critical 2 losing consciousness (supports integrated info theory)
