Lecture 18: Learning and Memory 2 Flashcards

1
Q

Engram

A

The neural representation of memories

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2
Q

Karl Lashley ( 1890-1958)

A
  • First researcher of brain mechanisms of learning and memory
  • Examined learning in rats following transactions (cuts of axons) and lesions (removal of brain matter) of different cortical regions
  • Cortical transactions failed to block learning
  • Cortical lesions slight learning impairments, and location did not really matter
  • Larger lesions led to more impairment
    “this series of experiments has yielded a good bit of information about what and where the memory trace is not”
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3
Q

Equipotentiality of Memory in the Cortex

A

All areas of the cortex are equally involved in memory

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3
Q

Patient H.M.

A
  • Suffered from epilepsy in the hippocampus as a child
  • Doctors removed the hippocampus and adjacent structures on both hemispheres
  • Epilepsy largely relieved
  • Lost the ability to form new episodic memory
  • Anterograde amnesia
  • Also suffered temporally graded (just before the removal of the hippocampus) retrograde amnesia
  • Could learn skilled movements
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3
Q

Mass Action

A

Ability to form memories depends only on the mass of brain matter

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4
Q

Synaptic Plasticity Hypothesis

A

Experience can leave a memory trace by causing long-lasting changes in synaptic connections

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4
Q

Long-Term Potentiation (LTP)

A
  • A potential mechanism for experience-dependent synaptic plasticity
  • Repetitive high-frequency (intense stimulation of a presynaptic neuron induces a long-term increase of the synapse with the postsynaptic neuron
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4
Q

Glutamate binding to AMPA receptors

A
  • Glutamate bings to AMPA causing a sodium channel to open
  • Results in depolarization (EPSP) in the postsynaptic cell
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4
Q

Trisynaptic Circuit of the Hippocampus

A
  1. Information about experience arrives into the hippocampus from the entorhinal cortex to the dentate gyrus through the performant pathway (LPP/MPP)
  2. info gets through mossy fibers (MF) to CA3 pyramidal cells
  3. Through schaefer collaterals (SF) info reaches CA1 pyramidal cells
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4
Q

Hebbian Plasticity (Learning)

A

If cell A persistently and repeatedly excited cell B, the efficacy of the synapse between them will increase

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5
Q

Glutamate binding to NMDA receptors

A
  • Opens a calcium channel
  • Molecule of magnesium blocks Ca2+ from entering
  • Strong and consistent depolarization in AMPA causes Mg2+ to leave
  • Ca2+ causes more AMPA to be produced via genes and more transport via second messenger cascades
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