3.3 neural processes: brain regions and neural mechanisms Flashcards

1
Q

what are 4 research methods to determine brain regions involved in WM?

A
  1. lesion studies
  2. functional neuroimagin studies (fMRI, PET, EEG)
  3. neurophiosological studies (extracellular recording of neurons)
  4. neuromodulatory studies (reversible inactivation or electrical stimulation of brain regions)
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2
Q

how is a sensory representation built?

A

sensory receptors

early processing stations

thalamus

primary sensory corticies

association cortex

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3
Q

role of PFC in WM?

A

central executive (focuses attention, ordering, inhibiting)

does not store content of WM

reciprocally connected to more posterior sensory regions of the brain

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4
Q

role of dorsolateral PFC in WM?

A

focuses spatial attention

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5
Q

role of ventrolateral PFC in WM?

A

left = phonological loop
right = visuospatial sketchpad

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6
Q

role of parietal cortex in WM?

A

spatial WM

holds the contents of WM, connects with PFC which controls these contents

right side = spatial info of objects in left visual field
left side = processes verbal info

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7
Q

role of temporal cortex in WM?

A

lateral temporal cortex = verbal WM

temporal cortex = visual WM

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8
Q

role of temporal cortex in WM?

A

verbal and visual WM

no spatial WM

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9
Q

role of hippocampus in WM?

A

HM had no hippocampus but had unimpaired WM

medial temporal lobe (MTL) may be involved when task demands exceed WM capacity

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10
Q

how has the neural mechanism of WM been elucidated throughout history?

A

history: higher mental functions belong to psychology and philosophy

discoveries: place theory, persistent activity in PFC in subject with no sensory stimulus, and later, state theory

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11
Q

what is PA?

A

persistent activity
- continuous firing of neurons during a delay period in the absence of a sensory stimulus
- first found in the PFC, now in other areas too

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12
Q

2 conditions for PA?

A
  1. PA must be stimulus-specific
  2. PA must be able to predict WM errors (PA interference should affect WM)
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13
Q

3 methods that provide evidence for PA?

A
  1. neurophysiology: continued spiking in neurons
  2. EEG: signal obserrved above certain brain regions
  3. fMRI: increased blood flow to regions of WM
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14
Q

who first recorded PA? how?

A

fuster & alexander, 1971

behavioural task
- rhesus monkeys were single-unit recorded during a delayed response task (cue, delay, response)

observations
- sustained firing of neurons in PFC into the delay period
- PA observed in some neurons that didn’t respond to the cue

implications
- persistent stimuli-specific firing = sensory info is still being coded in its absense

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15
Q

what did EEG studies reveal about PA?

A

EEG = global electrical activity

after presentation of an event, an event-related potential (ERP) can be visualized

visualize ERP by averaging activity across several trials to minimize noise.

EEG signals show synchronized activity of large populations of neurons = indicates level of alertness (commonly gamma rhythms in demanding tasks)

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16
Q

what findings have shown the localization of PA?

A

PA first in PFC + sensory association areas (parietal and temporal) = PA was holding the representation in WM

fMRI = PA is in primary sensory areas (primary visual cortex)

Dr. Martinex-Trujillo + electrophysiological studies = PA not observed in primary sensory areas, PFC and sensory-association areas only

17
Q

what are 2 theories about how PA is generated/maintained?

A
  1. neurophysiological mechanisms
  2. neural circuit mechanism
18
Q

what is the neurophysiological mechanism of PA?

A

intrinsic persistent firing

afterdepolarization = membrane does not return immediately, remains depolarized. if large enough, then persistent spiking may occur

calcium-dependent: PA has been shown to be sensitive to chelation of Ca2+

19
Q

what is the neural circuit mechanism of PA?

A

cell assemblies reverberate due to reciprocal connections

can set up oscillatory frequencies