W6L2 - Neuroanatomy & Biochemistry of Memory Flashcards

1
Q

What are extra-temporal connections to the MTL

A
  1. Papez Circuit
  2. Frontal Lobes
  3. Dienecephalon
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2
Q

What is the Limbic System and what does it regulate

A

Limbic System = Amygdala + Papez Circuit

  • Emotional expression and experiences
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3
Q

What is the role of the Amygdala in memory? What happens if it’s leisoned?

A

Role of Amygdala

  • Memory for emotionally arousing experiences (Not necessarily fear)
    • Fear conditioning
    • Rich representations of emotional experiences

Lesioned

  • Loss of conditioned fear
  • Impairment of new fear learning
  • Reduced memory for emotionally laden events (Not necessarily fear)
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4
Q

What are the parts of Papez Circuit (in order)

A
  1. Hippocampus
  2. Fornix
  3. Mamillary Body - Part of Hypothalamus
  4. Anterior Thalamus Nuclei - Part of Thalamus
  5. Cingulate Gyrus

[Closed Circuit]

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5
Q

What is the role of the Papez Circuit in memory? Lesion to which part is memory most reliably imparied?

A

Declarative Memory

General View

  • Relational memory/encoding, similar to MTL
  • Most reliable when hippocampus or ATN are leisoned. But other parts also cause relational damage
    • Damage tend to be spread anyways
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6
Q

What does the Frontal Lobe contain

A
  • Posterior Frontal Lobe
    • Motor and premotor cortex
    • Motor programming
  • Anterior Frontal Lobe
    • Prefontal cortex
    • Cognitive Control Processes
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7
Q

Leision of Frontal Lobes in Memory

A
  • Impairment in developing and implementing strategies for appropriate memory encoding and retrieval
  • Impairment in remembering contextual details (DLPFC)
    • E.g., Sources of information, chronological order of memories
  • Confabulation (VLPFC)
    • Production of statements involving bizarre distortions of memory
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8
Q

Where are the rich connections in frontal lobes connected to

A

Rich reciprocal connections:

  1. ) Within frontal lobes itself
  2. ) With MTL (hippocampus, neocortical association areas, etc)

(With hippocampus via fornix)

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9
Q

What is the Dienecephalon

A

Dienecephalon = Thalamus + Hypothalamus

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10
Q

What does the hypothalamus contain? Hence?

A
  • Mamillary bodies (In Papez Circuit)
    • Impairment = loss of declarative memory (relational)
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11
Q

What does the thalamus contain

A
  1. ATN (Papez Circuit)
  2. Mammillo-thalamic tract (MMT): Connects ATN with hipocampus
  3. Medio Dorsal Nuclei (MDM) / Dorsal Medial Nuclei
  4. Internal Medullary Lamina (IML) / Midline
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12
Q

Which parts of leisons of thalamus most likely to cause memory loss

A

Anterior and Medial

  • More likely
  • Most connected to frontal lobes
    • Anterior (part of Papez circuit)
    • Medial

Posterior and Lateral

  • Less likely
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13
Q

Damage of mammillo-thalamic tract (connects ATN to hippocampus) and ATN

A

Declarative (Relational memory)

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14
Q

Damage of Medio Dorsal Nucleus (MDN) and/or Internal Medullary Lamina (IML) damage; but spared mammillo-thalamtic tract (MTT)?

A

Specific retrieval difficulties

  • Impaired Recall
  • Preserved Recognition
    • Top Down cannot recall, but can recall under prompt
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15
Q

Damage of Medio Dorsal Nucleus (MDN) and Intralaminar/Midline Nucleus?

A

Medio Dorsal Nucleus

  • Deficits in selecting the appropriate information to be retrieved
    • ‘Active retrieval’

Intralaminar/Midline

  • Deficits seen in semantic memory, memory retrieval
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16
Q

Summary of leisions of the 3 areas

A
  • Papez’s circuit lesion
    • Impaired relational memory/encoding (Similar to MTL)
  • Frontal Lobes
    • Impaired ability to organise the encoding, retrieval and maintenance of memories
  • Dorso-medial, intralaminar and midline nuclei
    • Impaired memory due to reduced mental flexibility and inappropriate selection of information retrieval
17
Q

Biochemistry: What does learning require

A

Synaptic Plasticity

Biochemistry of synapses change to alter the effect on post-synaptic neuron

18
Q

What is LTP

A

Long-term increase in excitability of a neuron (B) to a particular synaptic input caused by repeated high frequency activity of that input (A)

19
Q

What is Hebb’s Law. What does it describe

A

When an axon of cell A…excites cell B by repeatedly firing it, change takes place in 1 or both cells to increase A’s efficiency

  • Describes long-term potentiation
20
Q

Evidence for LTP

A
  • Baseline EPSP measured for single electrical stimulus
  • 100 electrical stimuli delivered rapidly
  • Increased EPSP for subsequent single electrical stimulus
    • LTP
21
Q

Biochemically, how does LTP cause synaptic changes? Describe the changes at the level of the pre and post-synaptic

A

(Glutamate)

Pre-Synaptic

  • Increased glutamate by pre-synaptic terminal button

Post-Synaptic

  • New receptors
  • Increased receptor sensitivity to glutamate
  • Increase protein synthesis in post-synaptic dendrites
22
Q

Sites of LTP (Where it occurs)?

A
  1. ) Hippocampus (esp. dentate gryus + CA1), entorhinal cortex
  2. ) Others: Frontal Lobes, Thalamus, Amygdala, Visual Cortex
23
Q

What are 3 other mechanisms of neural plasticity

A
  1. ) Long term depression
  2. ) Habituation
  3. ) Sensitization
24
Q

How does Long Term Depression affect neural plasticity

A

Low frequency stimulation at synapse decrease synaptic strength

25
Q

How does Habituation affect neural plasticity

A

Repeated stimulation reduces strength of synaptic response (Reduced NT release)

Note: Repeated but neutral

26
Q

How does Sensitization affect neural plasticity

A

Single noxious stimulus causes exaggerated synaptic response to repeat presentation of noxious stimulus