Machado Flashcards
when talking abt brain scans (but Not gross anatomy)…
left + right r reversed
what makes up ur CNS (simple)?
spinal cord + brain
where does sensory info enter the CNS?
dorsal portion of the spinal cord
where do motor commands exit the CNS?
ventral portion of the spinal cord
what terms of orientation r used 4 reptiles thru-out the CNS?
dorsal, caudal, ventral, rostral
where do the terms of orientation (CNS) change 4 humans?
below the junction w the midbrain (diencephalic junction)
terms orientation above midbrain (human)?
- anterior = rostral (front of brain)
- posterior = caudal (tail/end of brain)
- superior = dorsal (top)
- inferior = ventral (bottom)
below midbrain terms of orientation (human):
- rostral (top)
- caudal (bottom)
- dorsal (towards back, like a fin)
- ventral (2wards stomach)
lateral def:
towards the side
medial def:
2wards the midline… get it.. med –> midline
ipsilateral
same side
contralateral
opposite side
where do most outgoing motor commands exit
on the opposite side!! contralaterally !!
terms 4 brain slices:
- horizontal (looking frm on top)
- coronal (straight thru the middle)
- sagittal (slice goes right thru midline of the brain, separates left n right hemispheres)
4 lobes of cerebral cortex (divided into 2 hemispheres):
- frontal
- parietal
- temporal
- occipital
insular cortex
situated between frontal + temporal lobes, revealed once you’ve removed cortex around the lateral sulcus
longitudinal fissure
separates left n right hemispheres, deeper than sulcus (but sometimes interchangeable)
lateral sulcus
separates frontal + parietal lobes frm temporal lobe
central sulcus
separates frontal lobe frm parietal lobe
major gyri:
- frontal lobe: superior, middle, inferior
- temporal: superior, middle, inferior
- parietal: postcentral gyrus, intraparietal sulcus (IPS) separates superior + inferior portions of lobe
which direction do the frontal lobe gyri run?
anterior –> posterior, meeting the pre-central gyrus at pre-central sulcus
what is the corpus callosum?
c-shaped bunch of axons crossing over n connecting the 2 hemispheres
where’s the cerebellum located
hangs off of the back/dorsal part of brainstem . looks like cauliflower
what r u Generally talking abt w cortical structures
hippocampus, cerebral cortex
what r u talking abt w subcortical structures
white matter, thalamus
what r the basal ganglia (in the broadest sense)?
lots of diff subcortical structures, main ones being: caudate nucleus, putamen, globus pallidus
what r the main structures in the basal ganglia generally made up of?
cell bodies, not axons
describe the shape of the caudate nucleus
c-shaped, head is the fattest bit n tail wraps around in2 the temporal lobe
brainstem structure overview
superior colliculus –> inferior colliculus –> pons –> medulla
where r the colliculi located?
hanging off back of midbrain, upper 2 bumps r superior; lower 2 r inferior
how many bumps 2 the colliculi?
4 :p
major divisions of the ventricular system:
lateral ventricles, 3rd ventricle, cerebral aqueduct, 4th ventricle
describe the ventricular system broadly
consists of interconnected cavities filled w CSF, helpful 4 orienting urself w brain scans
describe lateral ventricles
- largest of ventricles
- look like c-shaped horns, extend frm frontal lobe into parietal + temporal lobes . little end horns poke in2 occipital lobe
where do the lateral ventricles connect 2?
interconnected w the 3rd ventricle (which is the midline cavity)
where is the 3rd ventricle connected 2
connected w the cerebral aqueduct –> then connects 2 4th ventricle
where is ur 4th ventricle located
between cerebellum and brainstem
where does the 3rd ventricle sorta encircle?
thalamus
white vs. grey matter
white matter = axons, grey matter = cell bodies
what percentage do neurons make up of brain cells
abt 10% - glial cells account 4 abt 90% (mostly in supportive role)
basic structure of a neuron:
dendrites, soma (cell body), axon, axon terminals
what do dendrites do?
receive input frm other neurons, transmit message down neuron
purpose of neuron soma?
contains metabolic machinery that maintains the neuron
what makes axons white
being covered in myelin yayy
how r long r axons
<1mm to over a metre wow….
what do u call it when axons branch out !
axon collaterals (cause they’re collateral… extra.. accidental)
what forms myelin
oligodendrocytes (type of glial cell)
multiple sclerosis + myelin. GO
its a demyelinating disease (destroys oligodendrocytes –> impacts myelination of axons –> disrupts normal communication)
what r the two sides of a synapse?
- pre- and post-synaptic
- info flows frm presynaptic neuron 2 postsynaptic one (dendrites r postsynaptic cause they already have the info, positioned after the synapse)
what do synaptic vesicles contain
chemicals (e.g. dopamine), if a neuron communicates w dopamine NTs might say its dopaminergic
when is electrical signal in neurons translated in2 chem
@ axon terminal, then chem signal (NT) crosses synaptic cleft
when is chem signal translated back 2 chem
on post-synaptic membrane, the chem signal is converted back 2 electrical:)
what volume of brain do glial cells make up
a lil more than half of brain volume (smaller than neurons)
main types of glial cells in CNS:
astrocytes, oligodendrocytes, microglia
what do astrocytes do
form barrier between neuronal tissue n blood (BBB), protect CNS frm some molecules in bloodstream
how do oligodendrocytes form myelin
- by wrapping their cell membranes around axon during development
- myelinating 1 axon requires lots of oligos, but 1 oligo can myelinate more than 1 axon –> both sluts
microglia function
eat n expel debris left by dead or degenerating brain cells
what triggers synaptic transmission (synaptic vesicles spill content in2 synaptic cleft, excite next neuron)
action potentials
what does ‘neuron has fired’ refer 2
when a neuron undergoes an AP
what might spikes refer 2
how many APs fired per second
what causes an AP
rapid change in the voltage of cell membrane
how might an AP b elicited artificially
having an electrode inject current –> neuron goes woww guess i better fire
a rat moves 1 whisker. how many APs will somatosensory neuron fire per second?
abt 100
what’s a single cell recording in theory
picking up electrical activity frm one neuron
cell’s receptive field def:
all visually sensitive cells only respond 2 stimuli in a region specific 2 them - that’s their receptive field
background firing rate
how many times neuron wld fire without stimulation
maps of neural activity: monkey study (M1)
- while monkey viewing left stimulus, inject it w radioactive agent
- metabolically active cells in V1 absorbed agent –> showed that organisation of cells represented the visual field (like an image of what was being seen)
what tool do u use 2 look @ how many neurons r involved in the rep of 1 image?
- fMRI: records changes in metabolic activity, producing functional view of brain
- signal frm fMRI is roughly proportional 2 neuronal activity –> can use it 2 estimate no. of neurons involved in specific cognitive process
fMRI study (Levy et al., 2004)
- visual cortex scanned while participant viewed image (e.g. house)
- found: @ least 2 mil neurons involved in rep of one image
somatosensation
sensation frm the body
what defines tonotopic map in primary auditory cortex?
frequency tuning (e.g. neurons tuned 2 higher frequencies stick 2gether)
describe brain lesion analysis
- look @ how brain normally functions by investigating behaviour of patient w lesion in region of interest (ROI)
- compares patients w ROI lesion vs. no lesion in ROI
which has higher resolution - CT (computed tomography) or MRI?
MRI, cause its more modern
describe EEG
electrodes attached 2 scalp, signal detected by each electrode amplified n recorded –> provides recording of brain’s electrical activity
describe ERPs (event-related potentials)
signature of brain’s electrical activity in response 2 certain event
–> ERPs r averaged across trials (removes background noise)
–> true ERP found
ERP research looks @ electrical activity in response 2 an event in terms of:
- latency (earlier electrical activity = brain responding faster)
- amplitude (e.g. if looking @ Jen Aniston cells + present her face, wld have higher amplitude response/higher magnitude of electrical activity)
- polarity: positive vs. negative activity (up or down on graph)
- scalp topography: where activity is - but Not v precise
strengths n weaknesses of ERPs
poor spatial resolution, great temporal resolution (when activity occurred)
structural imaging types:
CT, MRI, DTI
functional imaging types:
PET + fMRI
describe CT
uses x-ray 2 produce series of brain images (old but common), helpful 4 determining damage 2 brain tissue
describe DTI (diffusion tensor imaging)
provides view of white matter tracts (i.e. axons) using MRI scanner
describe PET
- radioactive material enters bloodstream, goes 2 metabolically active areas of brain (firing the most)
- PET scanner provides image of concentration + distribution of radioactive agent (functional view of brain)
note: hot colours = lots of radioactive material; blue colours colours = none
note 2: bc just provides functional view, must b overlaid on2 structural image
fMRI description
- records metabolic-activity related changes in successive images –> functional view of brain
- better spatial resolution than PET
Neuroanatomical Correlates of Single + Dual-Language Picture Naming in Spanish-English Bilinguals study (fMRI):
- compared brain activity when engaged in bilingual or unilingual task
- found more activation (Broca’s Area) in bilingual condition
TMS (transcranial magnetic stimulation) description
- brief magnetic pulse causes brief disruption 2 brain activity
- disruption can b excitatory (e.g. when TMS coil held over right hemisphere + left hand moves) or inhibitory (e.g. when TMS coil held over right hemisphere + there’s difficulty moving left hand)
where do neurons in primary motor cortex control?
left hemisphere innervates left side of body; right hemisphere - vice versa
outer ear structure
- pinna: prominent fold of cartilage-supported skin, captures sound + focuses it into the auditory canal
- auditory canal ends @ eardrum
middle ear structure
- ear drum/tympanic membrane
- ossicles - middle ear bones
middle ear process
- when sound wave reaches middle ear, series of differing pressure regions impinge on eardrum (high pressure pushes eardrum inward, low pulls eardrum outward)
- continuous arrival of differing pressures causes eardrum 2 vibrate –> vibrate ossicles 2
- ossicle vibrations transmitted 2 inner ear fluid via vibration of membrane @ the oval window
inner ear structure n function explained
- cochlea (spiral-shaped, fluid-filled tube) contains hair/receptor cells
- vibrations in the cochlea produce waves in the fluid –> hair cells move –>
- convert mechanical signal into electrical, synapse on2 spiral ganglion cells in cochlea
describe spiral ganglion cells
cells r tuned 2 specific frequencies, cells that prefer same/similar sound usually clustered 2gether
tinnitus cause/s
disease processes affecting cochlea or auditory nerve OR spontaneous activity (transient, e.g. cause of loud gig)
inner ear + balance
- spiral ganglion axons exit cochlea + converge w vestibular axons –>
- form vestibulocochlear nerve, which carries nerve impulses 4 balance + hearing frm ear 2 brain
where do spiral ganglion cells in vestibulocochlear nerve synapse on2?
once @ brain stem, spiral ganglion cells synapse on2 neurons in the cochlear nuclei (located @ level of lower pons/upper medulla)
auditory pathways described
- frm cochlear nuclei, auditory info ascends bilaterally 2 inferior colliculi
- neurons in inferior colliculi synapse on2 neurons in the medial geniculate nucleus (MGN) of thalamus
- MGN neurons synapse on neurons in primary auditory cortex (A1)
thalamus described
large structure connected 2 top of brain stem, contains MGN
A1/Heschl’s gyri
- 1st region of cortex 2 process sound, located in superior temporal lobe n buried w/in lateral sulcus
- A1 organised by tonotopic map (maintained frm cochlea)
interaural time def
difference in arrival time of a sound @ each ear, can b used 2 determine location
sound localisation along the vertical plane is… ?
Nawt as good in humans
cochlear implants vs. regular hearing aids
- regular hearing aids amplify sound, cochlear implants have implanted electrodes (directly stimulate any functioning spiral ganglion cells w/in cochlea)
- cochlear implants have only abt 24 electrodes to replace 16k hair cells (not Great hearing experience)
do ur ears project auditory info in2 one or 2 hemispheres?
both, so still receive info even w damage to one ear
success of vision depends on which factors (broad)?
- localisation of light reflected off of distant objects
- object identification based on size, shape, colour, past experience
- movement detection
- compensation 4 changes in lighting conditions
pupil
opening that allows light 2 enter eye + reach retina (focuses light)
iris
circular muscle that controls size of pupil
cornea
transparent surface covering pupil + iris
sclera
eye white, continuous w cornea
lens
helps focus rays of light on2 retina
retina (basic overview + flow of visual info within it)
- rear 2/3s of eye, converts images into electrical impulses (then sent 2 brain)
- flow of visual info in the retina: photoreceptors → bipolar cells → retinal ganglion cells (their axons carry info frm eye 2 brain)
macula
central area of retina around fovea specialised 4 central vision
fovea
midpoint of retina, visual info received by fovea is the least distorted
optic nerve
consists of retinal ganglion axons, carries impulses 4 vision frm retina 2 brain
muscle of the eye - describe
have 3 pairs of extraocular muscles inserted in2 sclera, enable eye 2 move
what light waves can humans see
between 400-700nm
receptors of vision (broad)
- millions of photoreceptors in back of retina, two types: rods + cones
- on one end of both rods n cones is photopigment that absorbs light energy –> excites cell –> cell transmits info on2 bipolar cells
rods (properly)
- 4 low light levels (approx. 1k x more sensitive to light than cones)
- no colour vision
- rod-shaped
what do we primarily rely on 4 vision + why
centre of vision - has higher concentration of cones
does the peripheral retina have more rods or cones
more rods
cones (properly)
better for higher light levels, gives colour vision
what determines cone type
photopigment sensitivity 2 certain wavelengths
what r the 3 types of cones
blue, red, n green
structure of a cone
photopigment –> cell body –> synaptic terminals
what abt the photopigment in rods?
they have one type of photopigment w one sensitivity
how does light cum thru eye - not frm fovea
light cums thru pupil, projects 2 retina
–> light has 2 make its way thru other cells to get 2 photopigment (visual info gets a lil distorted)
how does light cum thru eye (fovea n macular region)
cellular processes (like RG cells) r pushed aside, light arrives 2 photoreceptors less distorted
organisation of like, the internal eye (photoreceptors etc)
nerve fibres –> ganglion cells –> bipolar cells –> photoreceptors
blind spot … explained…..
where axons of RG cells exit the retina, there r no photoreceptors (no visual experience) - but we dont notice cause brain fills in visual info
what is the optic nerve (simple)
RG axons sending info 2 brain, located @ optic disk
what does a lack of blood vessels in macular region mean 4 vision there
better vision (less clutter?)
nasal vs. temporal hemiretina
- nasal = closer 2 ur nose
- temporal = other hemiretina/closer to ur Temple
why does blind spot affect temporal hemifield
cause optic nerve fibres exit eye via nasal hemiretina
when do RG axons in the nasal hemiretinas cross over
@ the optic chiasm
do RG axons frm the temporal hemiretinas cross over
they do Nawt,,, so after optic chiasm, u end up w everything frm left hemifield on right side of brain n everything frm the right hemifield on the left
when does optic nerve become optic tract (now in CNS)
after optic chiasm….
what happens 2 vision if left optic nerve is cut
vision frm left eye will b lost completely, resulting in loss of left peripheral vision
what happens if optic chiasm cut/transected (affecting nasal hemiretinas)
peripheral vision lost bilaterally
what happens if left optic tract cut
lose all right hemifield vision
what is superior colliculus called in non-mammalian vertebrates
optic tectum
what is the subcortical visual pathway
the retinotectal pathway…. tectum = superior colliculus
describe retinotectal pathway (simple)
retina projects 2 superior colliculus
describe the retinotopic map of superior colliculi in the retinotectal pathway
- each superior colliculus has a map of opposite/contralateral hemifield
- retinotopic map is distorted, w more neurons devoted 2 analysis of central visual field
what percentage of RG axons project via the retinotectal pathway
abt 10%
what is the cortical vision pathway (simple)
retinogeniculostriate pathway… retina –> thalamus (lateral geniculate nucleus) –> V1/striate
what percentage of RG axons project via retinogeniculostriate pathway
abt 90%
overview of V1/striate cortex/area 17
- receives visual input thru thalamus
- 1st region of cortex 2 process visual info, has complete map of retina
- located in medial part of occipital lobe + buried w/ in the calcarine fissure
describe the retinogeniculostriate pathway (more in-depth)
each LGN receives info abt contralateral hemifield, contains visual maps –> project axons (optic radiation) 2 V1 (where there’s another retinotopic map of contralateral hemifield)
describe: study revealing V1 topography
injected monkey w radioactive agent while looking @ display (V1 cells firing wld be stained by agent) –> showed that display was in fact preserved
what happens when TMS placed over occipital cortex (broad)
- when placed over the occipital cortex, TMS elicits light sensations (phosphenes) in the absence of any visual stimuli
- minimum TMS intensity 2 evoke phosphenes is referred 2 as the ‘phosphene threshold’
- reduced phosphene threshold reflects increased visual cortex excitability; increased phosphene threshold reflects reduced visual cortex excitability
phosphene threshold explained
- minimum TMS intensity 2 evoke phosphenes referred 2 as phosphene threshold
- reduced phosphene threshold = increased V1 excitability; increased = reduced V1 excitability
ecstasy + V1 excitability (study)
- using excitatory TMs on ecstasy users
- comparing excitability of V1 4 users + non-users, hallucinators + non-hallucinators (w/ in ecstasy users)
- results: users had significantly lower phosphene threshold than controls, hallucinators also had lower threshold
is sensory info integrated immediately or later
later- initially transmitted 2 unimodal areas of cortex, then goes 2 hetero/multi-modal regions of cortex for sensory integration
give an example of where sensory integration might take place
for auditory info, inferior colliculi send info not only 2 MGN but Also superior colliculi (where visual n auditory info can b integrated)
ventriloquist illusion explained
when speech appears 2 come frm puppet’s mouth this is due 2 the sound source being mislocalized 2wards a synchronous but spatially discrepant visual event
where is Most sensory info relayed frm to the cortex
thalamus (LGN, MGN) –> cortex
what side of ur body wld right hemisphere neurons in primary motor cortex represent
the left side !!
response properties
what stimuli excite certain cells or neurons
area MT in monkeys is what in humans..?
area V5
pt.2 Macque monkey study: what did they do next?
once they discovered what direction of motion area MT neuron preferred, went w that + varied speed –> realised neurons also had speed preference
single-cell recording in area MT (pt.1 study on Macaque monkeys)
- single-cell recording done while white bar passed thru neuron’s receptive field in varying directions (trying 2 understand motion/direction sensitivity)
- results: neuron fired more when bar moved downward 2wards the left, opposite movement elicited least activity
–> area MT neurons sensitive 2 direction of motion
how might u use PETs 2 investigate specialisation of function in V1
since PET measures regional cerebral blood flow, can identify which paths of brain r involved in the perception of certain visual stimuli
using PETs 2 look @ which part of human brain is involved in colour processing (study)
- used abstract coloured scenes
- to remove background noise, activity elicited by abstract scene (grey) was subtracted by abstract scene (coloured)
- results: ventral area of extra striate cortex involved in colour processing
subtraction method
results frm experimental condition - results frm control condition
study: PET activation during visual stimulation (motion processing)….
- participants shown moving display (black n white square patterns)
- to remove noise showed stimuli not moving (subtraction method)
- results: dorsal area of extra striate cortex involved in motion processing
what r the 2 main projection routes frm V1 to extrastriate visual cortex?
- dorsal (motion + location; ‘where’)
- ventral (processes detailed stimulus features + object identity; ‘what’)
do the visual areas w/in extrastriate cortex contain maps of contralateral or ipsilateral hemifield?
contralateral !!!
where is V4 located, what does it do
located along ventral stream, once thought 2 only b important 4 colour processing but actually important 4 form/shape processing 2
where is V5 located, function
located along dorsal stream, selective 4 direction + speed of motion
how much brain power goes in2 cortical vs. subcortical visual processing?
LOTS more 4 cortical
r subcortical pathways colour blind yes or no . AND did they evolve earlier than cortical
YES !! and yes (phylogenetically older)
where r neurons that receive info frm RG cells located in the superior colliculi
superficial layers of superior colliculi
what did Goldberg & Wurtz (1972) do/find
- mapped receptive fields of neurons in superficial layers of superior colliculi (monkeys)
- used single-cell recording
- found: superficial layers of superior colliculi provide retinotopic map, each representing contralateral hemifield
what prompted the unilateral removal of visual cortex study
damaged cortical visual system in cat → cat cld no longer see contralaterally (cortically blind, specific 2 opposite hemifield)
what did unilateral removal of visual cortex study do/find
- by removing contralesional superior colliculus OR cutting fibres connecting superior colliculi, inhibitory fibres of superior colliculus wiped out → visual orienting returns
- known as Sprague Effect
why were subcortical visual pathways initially unable 2 compensate 4 damaged cortical visual system ?
bc ipsilateral superior colliculus needed 2 b released frm normal inhibition - which wld disinhibit subcortical pathway on side of cortical damage
explain Sprague Effect- why does it happen
results frm cutting inhibitory fibres that originate in another nearby structure + project 2 the ipsilateral (2 the cortical lesion) superior colliculus
study comparing effects of disrupting cortical vs. subcortical vision (rodents)
- group 1: bilateral removal of visual cortex
group 2: bilateral disruption of retinotectal pathway - findings (localisation): rodents w cortical damage unimpaired, subcortical damage impaired
- soooo subcortical visual system important 4 base visual orienting + cortical more useful 4 complex stuff
define double dissociation
groups have opposite pattern of results 4 same set of tasks
how might u assess the contribution of subcortical visual pathways (in the absence of cortical pathways) in humans?
by looking @ victims of stroke involving V1
perimetry testing
have patient fixate on centre, present light in diff positions + position says ‘yes’ until they can no longer see it
–>
maps out blind spot (scotoma)
what causes contralesional hemianopia
unilateral v1 damage
residual vision w/out V1? (Weiskrantz, 1986)
- used task that (unlike perimetry testing) didn’t require explicit report - instead tapped in2 patient’s implicit knowledge of their hemianopia field
- had patients w right V1 damage (left hemifield blindness)
- spot of light presented (don’t see it), then instructed 2 look 2ward where light was when tone sounds
- found: when spot of light appeared up to 20 degrees in2 blind field, responses were highly correlated w position of light (blindsight)
what might b responsible 4 blindsight Weiskrantz’s study
since V1 wiped out, subcortical visual pathways may have been responsible 4 blindsight
residual vision w/out V1 (2nd experiment, Rafal 1990)
- measured how quickly hemianopia patients patients cld look @ stimulus presented in their intact hemifield, depending on presence of irrelevant stimulus (distractor) in their blind spot
- results: eyes moved slower w presence of distractor in blind spot → can b explained by competing activation frm the distractor via the retinotectal pathway (subcortical visual system)
what is electromyography (EMG) + when might it pick up smth
picks up electrical activity associated w muscle activity (e.g. when eyes moved)
what is electrooculography (EOG) + when might it pick up smth
picks up electrical activity w moving eyes (finds neurons firing prior 2 + during eye movement)
what is the implication of being able 2 move ur eyes in pure darkness
since ur without visual stimulation in this situation, means u have some pure motor cells here (in the deeper superior colliculus layers)
do neurons in deeper layers of SC have a movement field (part of visual field that the eyes move 2 in response 2 cell activity; ‘motor map’)
yes, they have large movement fields
–> meaning each cell fires b4 a wide range of saccades (altho most intensely b4 saccades of their most preferred direction + amplitude)
movement fields of SC neurons code 4 eye movements in2 the contralateral hemifield. yes or no?
yes
movement fields tend 2 code 4 eye movements in2 the same area of visual field represented by the retinotopically organised visual receptive field of the neurons in the superficial SC layers. T or F?
True
how might u determine the movement field of a neuron in deeper SC layers?
thru electrical stimulation- wld evoke saccade in2 the movement field of the stimulated neurons
@ upper part of SC, have 0 amplitude movement (eyes dont move) → as u move down (rostral to caudal), get higher + higher amplitude. T or F?
True
reflexive saccade
rlly fast eye movement
effects of unilateral (right, in this case) SC damage on reflexive saccades in humans (study)
- latencies of reflexive eye movements were recorded
- found: contralesional saccades were delayed (when stimulus appeared opposite damaged SC) → SC helps 2 generate reflexive saccades 2wards stimuli that appear in the contralateral hemifield
how does a sudden change in visual periphery trigger a reflexive saccade?
visual info projects thru the retinotectal pathway to the SC → motor related activity in the SC then causes the eyes 2 rotate until the location of the visual change projects onto fovea
what r reflexive eye movements also referred to/why
exogenous eye movements - driven by external stimuli
where r the smallest saccades represented in the SC
smallest = rostral SC; largest = caudal SC
explain what fixation cells r
- when stimulus is present @ fixation point, cells in rostral portion of the superior colliculus r activated
- when fixation point disappears, firing rate of these cells declines –> they r fixation cells (underlie fixation reflex)
fixation reflex (simple def)
triggered by external visual stimulus projecting on2 central vision
difference between reflexive saccades + fixation reflex
- reflexive saccades help our eyes move in order 2 foveate a sudden change in the visual periphery, while fixation reflex helps eyes maintain their position
- ALSO, rostral cells + saccade cells inhibit each other (opponent processes)
how might u look @ the opponent process nature of the reflexive saccades + the fixation reflex
fixation offset effect paradigm
fixation offset effect paradigm (study)
- 2 conditions: fixation overlap (fixation dot + peripheral stimulus present @ same time), fixation offset (fixation stimulus disappears when peripheral stimulus appears)
- looking @ which condition will result in faster eye movement 2ward peripheral stimulus
- results: fixation offset faster
why is the fixation offset condition faster 4 eye movement 2ward peripheral stimulus?
cause when fixation stimulus disappears, fixation cell activity drops –> increased activity of saccade cells (less inhibition)
what’s the fixation offset effect formula
RT on overlap trials - RT on offset trials
what does FOE give measure of
how responsive ur fixation reflex is
–> large FOE indicates strong fixation reflex, small FOE = weak fixation reflex
FOE in young adults (result of 1 study)
20ms
what r endogenous eye movements
voluntary eye movements ! u don’t need external prompting
endogenous eye movement task
- fixate on centre until arrowhead appears
- move eyes 2 direction that arrowhead points
- after each response, turn eyes 2 centre + wait 4 next arrowhead
what were Ro et al. (1997) looking @
looking @ the contribution of the superior prefrontal cortex (SPFC) + superior parietal lobule (SPL) in generating voluntary + visually guided (exogenous) saccades
Ro et al. (1997): method + findings
- each ‘go’ signal presented w a TMS pulse (inhibitory - slowing down eye movements)
- TMS coil placed over either SPFC or SPL
- results: no effects, except when TMS was over SPFC 4 endogenous eye movements directed contralaterally
what was hypothesised frm the results of Ro et al. (1997)
- was hypothesised 2 b a consequence of disrupting the normal operation of the frontal eye field (FEF)
- however, still cannot b certain that TMS pulse disrupted FEF activity → need more experimentation
effects of a lesion involving the FEF on voluntary saccades (Henik et al., 1994)
- experimental group all had damage to one FEF
- results: patients w a FEF lesion had delayed voluntary saccades 2ward contralesional hemifield
–> FEF normally involved in generating voluntary saccades
do Henik et al. (1994)’s findings support Ro et al. (1997)’s theory
yes, they support his theory that delayed contralateral endogenous saccades caused by TMS over SPFC were a consequence of disrupting the normal FEF operation
exogenous vs. endogenous eye movements
exogenous eye movements depend more on subcortical structures, endogenous eye movements depend more on cortical structures
–>
FEF (cortical) receives info indirectly, has less direct projections down → so, reflexive faster (require fewer neural connections since less processing required)
what sort of structures r babies believed 2 have @ birth?
mature subcortical structures, but not fully developed cerebral cortex (cortical systems)
FOE experiment (Hood & Atkinson, 1993) - most important findings
- results: compared 2 older infants, 1.5-month-olds have slower responses on fixation overlap trials
→ fixation reflex stronger in 1.5-month-olds - so: maturation of cortex in older babies may have given them more control over fixation reflex
–> more specifically, maturation of cortico-subcortical pathways might b behind shift frm predominantly exogenously controlled orienting (in 1.5mos) 2 increasing endogenous control (in older babies)
@ how many months of age did Hood & Atkinson (1993) find infants 2 exhibit prolonged periods of fixation w some apparent difficulty in looking away frm fixated stimuli
abt 1-2 months of age
why might newborns exhibit a poverty of strategic behaviours (instead controlled largely by external stimuli)
immaturity of the frontal cortex -
frontal lobe not developed until 15-20yrs, performance on tasks requiring strategic control may continue 2 develop thru 20s
anti-saccade task
- fixate on centre, when stimulus appears look away frm it (this requires inhibition of a reflexive saccade, followed by execution of a voluntary saccade)
- performance assessed by: errors in the direction of the saccade (i.e. erroneous reflexive eye movements) + RTs (4 correct responses only)
- abnormally slow RTs suggest struggle imposing voluntary control (including over reflexive behaviours), high percentage of reflexive eye movements also suggest difficulty imposing voluntary control over them
age-related performance on anti-saccade task (Fischer et al., 1997)
- participants aged 9-20
- youngest children making Lots of reflexive errors (more than half of trials)
–> between 9-15, rapid decrease in frequency of direction errors (60 → 22%)
–>
RTs also decreased
age-related performance on anti-saccade task (Munoz et al., 1998)
- starting frm 5 years old
- results:
-dramatic improvement in the performance of anti-saccades between the ages of 5-15 years
-children aged 5-8 had most direction errors (erroneous reflexive saccades)
effects of lesion involving the FEF on anti-saccades (Machado et al., 2004)
- damage 2 one FEF
- anti-saccade task, measured variable was percentage direction errors
- results: had most difficulty when contralateral damage 2 stimulus presentation
(difficulty imposing voluntary control over reflexive eye movements)
what hypothesis do Machado et al. (2004)’s results support? n what does this mean
hypothesis that the FEF normally imposes inhibitory control over ipsilesional circuitry that generates reflexive saccades
–> so:
difficulty in inhibiting contralesional reflexive eye movements in patients w unilateral lesion involving the FEF cld reflect impaired modulation of activity in ipsilesional SC
which hemifield does each SC control reflexive eye movements towards
each SC controls reflexive eye movements 2ward contralateral (opposite) hemifield
after receiving info frm the retina, where does the SC project to?
projects 2 the saccade generators (SGs) in brain stem
how does the FEF receive info + where does it project 2
receives info indirectly, also projects down 2 SGs
where is FEF located
@ intersection of the superior frontal sulcus + precentral sulcus
do younger or older adults have less anti-saccade direction errors
young adults have less direction errors, smaller RTs too
frog brain has high proportion of subcortical neurons . is it more reflexive or endogenous in eye movements
reflexivee
what is an example of an exogenous attention task (hint: suns)
find the red sun amongst the green ones !
example of endogenous attention task (hint: also suns)
find red sun- but amongst not only green colours, but also red (have to use strategy, not reacting reflexively)
overt vs. covert shifts in attention
- overt - movement of eyes 2 shift attention
- covert - eyes dont move, but attention still shifts
ERP experiment in healthy adults
- looking @ activity in occipital lobe when stimulus appears in place participant is paying covert attention 2 (attention is directed voluntarily here) vs. in place where they r Not
- results: stronger neuronal signal occurred in response 2 stimulus when attention was directed there
→
selective attention 2 one part of visual field means neglect of other parts
r SC important 4 exogenous or endogenous shifts in attention
exogenous !!
what is true 4 results of both endogenous + exogenous attention tasks?
attention facilitates response (can respond more quickly)
what happens when u have an exogenous cue followed by a long delay?
after abt a second, actually respond slower - disadvantageous to have had attention drawn there
–>
a.k.a. inhibition of return = if ur attention is drawn somewhere + nothing happens, ur visual system inhibits attention in the future
is stronger or weaker inhibition of return (IOR) associated w better driving performance
stronger!!
when does the formation of CNS occur
during prenatal development
purpose of Flanker Task ?
2 assess efficacy of strategic control over attention (i.e., how easily distracted the participant is)
describe what happens during Flanker Task
- maintain fixation on screen centre
- when stimulus appears @ centre, indicate its identity by pressing the appropriate button ASAP
- 2 conditions: incongruent (participant is supposed 2 click ‘k’, but there’s an ‘s’ where ur not supposed 2 b paying attention; congruent (distractor is of the same letter as stimulus u shld b focusing on)
what is the Flanker Effect
RTs on incongruent trials minus RTs on congruent trials
what does the Flanker Task find 4 young vs. older adults
- younger adults slowed down by 23ms w distractor
- older adults slowed down much more (larger Flanker Effect), ageing associated w worse driving performance
→
according 2 these findings, cld b bc more easily distracted
what r the 3 main steps of brain development (just naming, not describing)
- cell division
- cell migration
- cell differentiation
outline cell division
- stem cells in CNS divide in2 two cells
- after dividing, newly divided cell migrates 2 take up position in cortex + stem cell remains 2 undergo more divisions
- stem cells divide until all the neurons of the cortex have been generated
outline cell migration
- new cell migrates by slithering along thin fibres that radiate 2ward brain surface
- cortical layers formed frm the inside out
once cells r in proper place, differentiation occurs. describe this .
process by which the newly divided cells take on the appearance + characteristics of a neuron or glial cell
what does neural plasticity refer 2
ability of nervous system 2 change
how does the level of overlap in the neural projections frm the eyes progress frm birth 2 some months of sensory experience
@ birth projections r quite overlapped, but later become more separated
ocular dominance columns def:
stripes of neurons in the visual cortex that respond preferentially 2 input frm a certain eye
describe formation of ocular dominance columns in V1
- @ birth, input frm the LGN representing both eyes r mixed in V1
- w early postnatal development, the input frm the eyes segregates in2 ocular dominance columns
what happens if you surgically rewire the brain 2 direct visual input 2 the auditory system? (von Melchner et al., 2000)
- looking @ newborn ferrets
- rewired hemisphere so that it went: retina → medial geniculate nucleus (MGN) → A1
- results: once adults, A1 neurons in the rewired hemisphere behaved like visual neurons in response 2 visual stimuli (e.g. had retinotopic organisation) AND when they disrupted cortical visual pathway thru lesioning, ferrets cld still see !!
effects of stimulating visual cortex in adults w impaired vision (study)
- all participants visually impaired due 2 damage b4 LGN
- measure: self-reported experience of phosphenes elicited by TMS over visual cortex (did u experience light flash)
- results: ppl w least impairment all experienced light flash, 60% who had poor residual vision, 20% w no residual vision
what do the results of the ‘stimulating visual cortex in adults w impaired vision’ study indicate
effect of activating visual cortex is altered in ppl w severe visual impairment
which brain structure is activated during mental imagery in sighted versus congenitally-blind adults? (study)
- participants either blind frm birth or sighted + blindfolded
- measures: looked @ brain activity using fMRI during passive listening 2 abstract words + subtracted that frm brain activity during mental imagery task
- results: both groups showed V1 activation
what is an example of functional plasticity in A1 (monkeys)
training monkeys 2 discriminate specific tone frequencies leads 2 enlargement of the cortical regions where the trained frequencies r represented
describe a study that demonstrates the plasticity of human primary motor cortex (M1)
- participants used non-dominant hand 2 perform finger to thumb tapping sequence
- two conditions: practised vs. unpractised sequences
- fMRI used 2 measure M1 blood flow under the respective conditions
- results:
- 3 wks practise: there were greater changes in blood flow in the contralateral M1 4 practised sequences (as compared 2 unpractised)
- 8 wks after final training: greater changes persisted in the contralateral M1 4 practised sequences
what happens when u have less plasticity of brain + atrophy
ur memory function declines! which has been connected 2 age-related reductions in size of hippocampus
ageing brain + aerobic exercise (study)
- lasted over 1 yr, assigned 2 aerobic exercise or stretching
- results: engagement in aerobic exercise can increase hippocampus size, improve accuracy of spatial memory
