lecture 5 - perturbation methods Flashcards

1
Q

accidental perturbations

alzheimer’s

A

tangles & plaques in limbic and temporoparietal cortex

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2
Q

accidental perturbations

parkinson’s

A

loss of dopaminergic neurons

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3
Q

accidental perturbations

huntington’s

A

atrophy of interneurons in caudate and putamen of the basal ganglia

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4
Q

accidental perturbations

picks

A

frontotemporal atrophy

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5
Q

accidental perturbations

disadvantages of accidental perturbations

A

not the most useful in making inferences about healthy human brain localization because atrophy likely to be widespread

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6
Q

accidental perturbations

chronic traumatic encephalopathy (CTE)

A

atrphy related to continued head trauma

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7
Q

brain lesions

brain lesions advantages

A
  • shows localized functions
  • can ask what consequences/changes are
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8
Q

brain lesions

surgical extirpation

A

cut out tissue of interest - irreversible

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9
Q

brain lesions

electrical lesions

A

heat tisse with strong electric current - irreversible

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10
Q

brain lesions

chemical lesions

A

injection of neurotoxins
- irreversible - kill neurons (ibotenic acid)
- reversible - temporary dysfunction (lidocaine)

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11
Q

brain lesions

cryogenic lesions

A

freeze a section of tissue - reversible

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12
Q

brain lesions

assumptions

A
  1. brain injury is eliminative, damage causes dsyfunction
  2. cognitive capacities can be analyzed into elemental (low-level) processes that underlie the capacity
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13
Q

brain lesions

single vs double dissociation

A

brain lesion impairs one function but not another
vs
one lesion impairs A not B, other impairs B not A

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14
Q

brain lesions

translation

concerns

A

are animals/patients good models/telling of healthy human brain function?

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15
Q

brain lesions

specificity

concerns

A

do we know the precise boundaries of the lesions?

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16
Q

brain lesions

compensatory mechanisms?

concerns

A

has damage caused reorganization/plasticity?

17
Q

brain lesions

behavioral complexity

concerns

A

are complex functions precisely located/ tied to one area?

18
Q

electrical perturbation

cortical stimulation

Fritsch & Hitzig

A

electrode implants on surface of brain (cortex)

19
Q

electrical perturbation

optogenetics

A

opsin inserted through genetic modification of cell populations, activation/deactivation of neurons w/ light

20
Q

electrical perturbation

deep brain stimulation

A

electrode insertion into deep brain tissue
ex: sub thalamus nucleus insertion to treat Parkinson’s

21
Q

non-invasive methods

transcranial magnetic stimulation (TMS)

A

delivering magnetic pulse through & across skull (superficial cortex) to disrupt neural activity

22
Q

non-invasive methods

observable effects of TMS

A

directed @ motor cortex, elicits observable muscle twitch or “motor evoked potential”

23
Q

non-invasive methods

online TMS

temporary lesion

A

establish timing of particular cognitive process and disrupt it
- one well timed pulse, double pulse, or short train of pulses

24
Q

non-invasive methods

offline TMS

A

extended electrical effects with extended stimulation
- 1-10 min period @ 1Hz pulse rate

25
# non-invasive methods TMS experimental considerations/disadv.
1. inability to penetrate too deeply, limited to cerebral cortex 2. possible downstream effects b/c of interconnectivity 3. can be uncomfortable
26
# chemical perturbation - neuropsychpharm drug alteration
exogenous compounds bind to postsynaptic receptors
27
# chemical perturbation - neuropsychpharm agonists
similar structures as NTs, mimics NT action
28
# chemical perturbation - neuropsychpharm antagonists
block or attenuate neurotransmission
29
# genetic perturbations knockout technique
genetic engineering to temporary turn off (reversible) or delete (irreversible) specific gene(s) examines consequences of lack of gene coding for particular protein
30
# genetic perturbation example of knockout technique
turn off gene that expresses transmembrane receptor like NMDA (glutamate)