Limbic system - Restrepo Flashcards

1
Q

Declarative memory. What is it? Where is it?

What structure is important to the formation of declarative memories, but not their storage.

A

Facts and figures.

Neocortex (different parts).

Hippocampus needed to create these memories, but not to store them (destruction of the Hippocampus results in anterograde amnesia).

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2
Q

What is procedural memory? What structures are needed to form them?

A

Procedural memory is motor memory.

Cerebellum, striatum, frontal cortex.

Recall that HM can learn motor skills, but cannot remember learning them (has procedural but not declarative memory).

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3
Q

Define short-term memory.

A

Short-term memory is considered memory that lasts for fractions of a second to seconds. Most sensory systems include this type of memory, and the processes underlying this type of memory takes place in sensory cortex.

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4
Q

Bob cannot remember whether he has put salt in the soup, so he does it many times and the soup is too salty. What kind of memory is missing?

Where are these types of memories stored

A

Working memory. (eg where are my keys)

Frontal cortex.

[FTD - have problems with working memory and executive function, both are frontal cortical lesions]

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5
Q

Define long-term memory.

A

Finally, memory that lasts for days and years is long-term memory, and it is stored in cortex (an example is memory for faces discussed above).

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6
Q

Describe the neuronal circuitry in the hippocampus.

A

Inputs from many sources pertaining to memory arrive at the ENTORHINAL complex (smell, vision, etc). The entorhinal complex follows the PERFORANT path, synapsing on the dentate gyrus and CA3.

The OUTPUT pathway takes impulses from CA1 and CA3, forming the fornix.

The CA1 is connected to the CA3 via the Schaeffer collateral axons. CA3 also receives inputs from the mossy fibers.

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7
Q

CA3 and CA1 are part of what larger anatomic structure?

A

Ammon’s horn.

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8
Q

You have an electrode attached to the perforant path neurons, or to Schaffers collateral axons. To what type of stimulation must you subject these pathways in order to produce LPT?

What happens after this stimulus is administered?

What 2 principles are derived from this experiment?

A

Tetanic stimulus (>100Hz).

After a tetanic stimulus, the EPSPs are larger.

1) Only the stimulated synapses will be potentiated
2) The tetanic stimulus must be large enough to cause a depolarization in the postsynaptic neuron

–> I.E. need Glu + Depolarization = NMDA receptors are involved.

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9
Q

How is alzheimers implicated with LPT, experimentally?

What therapeutic strategies does this suggest?

A

Transgenic mice that express beta-amyloid show a failure to maintain LPT in the hippocampus.

So Ab against BetaA, or enzyme inhibition of the beta/gamma secretase could be therapeutic strategies.

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10
Q

Describe the pathway that allows for Conditioned Flavor Aversion? Explain the time delay that allows for this response.

What drug category can block this response?

A

The basic response is still mediated by the NMDA receptor. The major difference is that eating a new food stimulates cholinergic release of AcH into the INSULAR CORTEX phosphorylates the NMDA receptor, which “props open” the channel. This opens a time window during which VAGUS nerve information can be transmitted through the AMYGDALA to the insular cortex, which would provide the glutamatergic stimulus to potentiate the relevant synapse.

Muscarinic antagonists can block this response.

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11
Q

What recent finding involving adult learning is inconsistent with the old theories?

A

New neurons in the dentate gyrus of the hippocampus form. Their function/involvement is unclear.

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12
Q

What condition occurs after removal of the amygdala?

A

Kluver-Bucy syndrome.

  • -> absent fear response (not afraid of snakes anymore)
  • -> inappropriate sexual drive
  • -> motivation
  • -> attention
  • -> eating non-food items
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13
Q

Describe the biochemical cascade triggered by the NMDA receptor when glutamate + depolarization are present.

A

Glu + depolarization–> Ca2+ influx into the cell–> stimulates calmodulin–> CAMKII autophosphorylates–> incorporation of AMPA receptors and phosphorylation of AMPA receptors –> increased EPSP

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