Synapses and Plasticity Four Flashcards

1
Q

What does LTD stand for?

A

Long Term Depression

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2
Q

What is special about synapse strength?

A

It is dynamic meaning that it can both be increased and decreased when needed.

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3
Q

What is a benefit of LTD?

A

Prevents saturation and loss of plasticity.

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4
Q

Since synaptic plasticity is dynamic what does this mean for the hippocampus?

A

Short term memory (hippocampus) is dynamic

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5
Q

In terms of onset of LTP and LTD what is different?

A

LTP is instant, LTD waits for the stimulation to finish occuring, over a period of 6-10minutes before happening.

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6
Q

what is LTD?

A

Activity Dependent decrease in synpatic strength

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7
Q

How is LTD incduced?

A

Low frequency stimulation for 5-10mins (1hz)

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8
Q

What is LTD dependent on?

A

Input specific- only synapses that are stimulated are depressed

Ca influx through NMDA receptors

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9
Q

What is the mechanism for LTD?

A

Low frequency stimulation for 5-10mins. Causes low levels of Ca to influx. This activates protein phosphotase which dephosphorylates AMPA receptors removing them from the membrane, decreasing the current flow during a synapse = decreased strength

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10
Q

What is membrane potential proportional to?

A

Ion flow through the channels on the post synaptic cleft. ie few receptors= little depolarisation can occur.

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11
Q

What determines of LTD or LTD occurs?

A

The quantity of Ca influx through NMDA- dependent on Glutamate release… and post synaptic depolarisation

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12
Q

What model is used to explore LTP and LTD?

A

Mice and humans are alive and used to explore LTP and LTD

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13
Q

What are four factors for exploring LTP and LTD in learning and memory?

A

1) LTD and LTP are induced using stimulation paradigms that are known to occur in vivo
2) WE know LTP and LTD occur in all major pathways involved in learning and memory (hippocampus, cerebellum, visual cortex)
3) Drugs that block LTP/LTD in the slice also prevent learning (NMDA blockers, Genetically removing camkII)
4) Enhancing synapses, results in enhanced plasticity and increased memory.

i.e increased NMDA receptors in transgenic mice = increased learning and memory

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14
Q

Can we record plasticity?

A

WE can do in vivo recordings of AMPA receptors moving = synaptic plasticity

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15
Q

Can we test synaptic plasticity and disease?

A

Yes we can breed animal models to have Developmental disorders such as down syndrome autism or Neurodegenerative diseases such as alzhiemers, parkinsons, huntingtons.

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16
Q

Why would we breed mice with these diseases?

A

AS they all exhibit learning, memory and plasticity deficits (less or more LTD or LTP)

17
Q

What are the remaining challenges for making the causal link between plasticity and learning/memory?

A

Difficult to record the same synapses that are undergoing plasticity and the ones responsible for memory.

18
Q

What are the phases of LTD?

A

Induction
Expression
Maintenance