Anatomy and neurobiology of memory: L12 Flashcards

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1
Q

role of amygdala in memory

A
  1. supporting memory for emotionally arousing experiences
    - fear conditioning
    - representations of emotional experiences
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2
Q

lesions of amygdala result in

A
  • loss of conditioned fear and impairment of new fear learning
  • reduced memory for emotionally laden events
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3
Q

what 3 regions of the extra-temporal brain are particularly involved in memory?

A
  • papez’s circuit
  • frontal lobes
  • diencephalon
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4
Q

what did James Papez propose in 1937

A

a specific brain circuit was devoted to emotional experience and expression
(Papez circuit + amygdala = limbic system)

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5
Q

what does papez’s circuit comprise of?

A

maxillary bodies, fornix, anterior thalamic nuclei (ATN), cingulate gyrus and the hippocampus

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6
Q

what is the efferent pathway?

A

outgoing, leaves the hippocampus -> fornix -> maxillary bodies. An efferent projection is then sent to the anterior -> cingulate cortex

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7
Q

what do lesions to papez’s circuit result in?

A
  • declarative memory impairment (poor relational memory/encoding)
  • declarative memory impairment most likely when hippocampus or ATN are lesioned
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8
Q

frontal lobes are involved in (1)

A
  • memory processing

- motor programming and function

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9
Q
  1. central sulcus location

2. primary motor cortex location

A
  1. line dividing frontal and occipital lobes

2. front side of the central sulcus = most posterior component of the frontal lobes

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10
Q

define homunculus

A

how the neuronal structure of the primary motor cortex and the primary somatosensory cortex are laid out

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11
Q

frontal lobes are involved in (2)

A
  • cognitive control processes e.g. problem solving, planning, monitoring and self-correction
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12
Q
  1. pre motor area

2. prefrontal area

A
  1. planning motor functions

2. executive cognitive processes

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13
Q

what are the frontal lobes involved in regarding memory? (Simons & Spiers)

A
  • developing and implementing strategies for appropriate memory encoding and retrieval
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14
Q

Damage to DLPF (area in frontal lobes) results in

A

misrepresentation of the chronological order of memories

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15
Q

Damage to prefrontal cortex can experience

A

confabulation = production of statements involving bizarre distortions of memory

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16
Q

Frontal lobe memory involvement

A

connections go directly back and forwards to the perirhinal cortex and the hippocampus via the fornix

17
Q

define diencephalon

- comprises?

A
  • interbrain = thalamus and hypothalamus
18
Q

what is the thalamus?

A
  • cortical connections of thalamus send reciprocal projections to different parts of the brain
19
Q

damage to particular area of thalamus results in?

A

severing the connection to its corresponding section of the brain

20
Q

Thalamus and memory

Van der Werf study results

A
  • anterior and medical lesions more likely to cause memory deficits than posterior or lateral lesions
  • dense amnesic syndrome associated with mammillo-thalamic tract damage
21
Q

what did cases with medio dorsal nucleus (MDN) and/or internal medullary lamina (IML) damage but spares MTT show?

A

specific retrieval difficulties (preserved recognition)

22
Q

damage to thalamus:

  • dorsal medial
  • intralaminar/ midline
A
  • dorsal medial, midline and intralaminar nuclei of the thalamus = role in memory
  • deficits in selecting the appropriate information to be retrieved ‘active retrieval’
  • deficits seen in semantic memory, memory retrieval
23
Q

axon hillock threshold needs to reach what for an AP to fire

A

55mV

24
Q
  • resting membrane potential is?

- undershoot is

A

-70mV

under -70 mV

25
Q

whats an excitatory post synaptic potential?

A

when a neurotransmitter crosses the synaptic cleft and produces an excitatory change in the dendrite (= increasing the voltage)

26
Q

what is synaptic plasticity?

- whats long-term potentiation?

A
  • the biochemistry of synapses change to alter the effect on post-synaptic neuron
  • a long term increase in the excitability of a neuron to a particular synaptic input caused by repeated high frequency activity of that input
27
Q

what’s Hebb’s rule?

A
  • when an axon of cell A excited cell B & repeatedly or persistently takes part in firing it
  • growth process or metabolic changes occurs in one or both cells
28
Q

Long-term potential (LTP)

A
  • the effect of cell A sending a message to cell B
  • baseline EPSP measured for single electric stimulus
  • 100 electrical stimuli delivered rapidly
  • increased EPSP for subsequent single electrical stimulus = LTP
29
Q

LTP causes synaptic change

A
  • additional receptors are inserted in the post synaptic membrane = more receptors for neurotransmitters to lock into
30
Q

LTP: what changes occur in synapses?

A
  • increased sensitivity of receptors to glutamate
  • increased amount of glutamate released by the pre-synaptic terminal button
  • protein synthesis in post-synaptic dendrites
31
Q

sites of long-term potentiation

A
  • hippocampus
  • entorhinal cortex
  • prefrontal cortex
  • motor cortex
  • thalamus
  • amygdala
  • visual cortex
32
Q

other mechanisms of synaptic plasticity

A
  • long term depression (low frequency stimulation = decreases synaptic strength)
  • habituation ( repeated stimulation -= reduces strength of synaptic response)
  • sensitisation (single noxious stimulus = exaggerated synaptic response)