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Physl > Nervous System 4 - Experiments and Mechanisms > Flashcards

Nervous System 4 - Experiments and Mechanisms Flashcards

1
Q

What is Synaptic Transmission modified by?

A

By past activity and by behavioural experiments

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2
Q

What is Synaptic Plasticity?

A

The capacity to alter the physiological strength of a transmission

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3
Q

What are the two forms of Synaptic Plasticity?

A

Short term and Long term

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4
Q

What are Short term and Long term plasticity distinguished by?

A

Their durations (from seconds to hours and days) and by the underlying molecular mechanisms

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5
Q

What does Short Term Plasticity entail?

A

Local changes of the synapse

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6
Q

What does Long Term Plasticity ential?

A

Changes in protein synthesis and gene transcription

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7
Q

What is a good measure of Synaptic Strength?

A

Amplitude of EPSP

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8
Q

What is a good measure of Synaptic Plasticty?

A

Changes in EPSP amplitude

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9
Q

What is Long Term Potentiation (LTP)?

A

A form of synaptic plasticity that involves strengthening of the synapses

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10
Q

What do many of the synapses in the hippocampus show?

A

Long Term Potentiation

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11
Q

What is Consolodation?

A

When short term memory gets converted into long term memory

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12
Q

What is the most intensively studies pathway in neuro research?

A

The Schaffer Collateral

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13
Q

What is Tetanus?

A

Intense stimulation at a high frequency

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14
Q

What does Tetanus cause?

A

It cause the EPSP to increase causing synaptic strength to be boosted

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15
Q

Why can LTP only be seen in the pathway that was stimulated?

A

Because LTP is pathway specific

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16
Q

Why is it important that LTP is pathway specific?

A

Because if it wasn’t LTP would saturate all the circuits and not allow for anymore plasticity

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17
Q

How long can LTP last for?

A

For several hours in a sliced hippocampus and for more than a year in intact animals

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18
Q

What is the Primary Excitatory neurotransmitter?

A

Glutamate (Glu)

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19
Q

Which receptors does Glutamate (Glu) bind to?

A

NMDA and AMPA receptors

20
Q

What are NMDA and AMPA receptors named for?

A

Synthetic chemicals that were designed to identify these receptors

21
Q

What happens when glutamate reaches a postsynaptic neuron at rest?

A

It binds with AMPA and NMDA receptors. The AMPA receptor allows sodium to enter while the NMDA receptor is blocked by Mg+

22
Q

What happens once Glu binds to AMPA and NMDA receptors in the postsynaptic neuron?

A

AMPA allows sodium to enter the cell while NMDA is block by Mg2+

23
Q

What is needed to unblock NMDA receptors?

A

The postsynaptic membrane has to be strongly depolarized and glutamate must be bound to it

24
Q

Why are NMDARs specialized?

A

Because they are both voltage dependant and chemically activated

25
Q

What happens to NMDARs once the membrane is strongly depolarized and glutamate is bound?

A

The Mg is expelled from the channel and Calcium and Sodium ions are able to depolarize the cell

26
Q

Why are NMDARs coincidence detectors?

A

Because they require to events to occur simultaneously in order to be activated

27
Q

Which proteins does a Silent synapse have?

A

NMDARs

28
Q

What proteins does a Functional synapse have?

A

AMPARs and NMDARs that develop through maturation of the brain

29
Q

What shows evidence of Silent synapses?

A

When the cell is clamped at -65mV (rest) no postsynaptic current occurs because the synapse only contains NMDARs which cannot conduct because Mg blocks the channel. But at +55mV (depolarization) the Mg block is removed and now current occurs

30
Q

What causes AMPARs to be inserted into a previously silent synapse?

A

LTP

31
Q

When AMPARs are activated what does it allow into the cell?

A

Sodium and Calcium

32
Q

After Calcium enter the cell through AMPARs where does it go?

A

It goes to activate CaMKII

33
Q

What does CaMKII stand for?

A

Calcium/Calmodulin protein Kinase II

34
Q

What does CaMKII do?

A

It phosphorylates proteins like AMPARs

35
Q

Why is the Phosphorylation of AMPARs important?

A

Phosphorylation of AMPARs is key for maintain LTP

36
Q

What would happen if CaMKII is blocked?

A

LTP initiation cannot occur

37
Q

How does CaMKII work in the cell?

A

Once calcium enters the cell through NMDARs it becomes activated and phosphorylates AMPARs and brings them to the cell membrane which allows for easier depolarization because they are only depolarized by glutamate

38
Q

What does adding AMPARs do?

A

Increases postsynaptic strength

39
Q

How does protein synthesis affect LTP?

A

Protein synthesis is required for maintenance of LTP

40
Q

How is protein synthesis initiated in order to produce AMPARs?

A

Protein kinases initiate cAMP which initiate Protein Kinase A which initiate CREB which is a transcription factor that allows for new synapses to grow

41
Q

What is Long Term Depression (LTD)?

A

Weakening of synaptic strength (smaller EPSPs)

42
Q

What can induce LTD?

A

Low frequency stimulation

43
Q

How does Low frequency stimulation induce LTD?

A

They involve the activation of phosphates which dephosphorylate proteins and remove AMPARs from the membrane

44
Q

What will factors that activate protein kinases or inactivate phosphates do?

A

Promote LTP and reduce LTD

45
Q

What will factors that activate phosphates or inactivate kinases do?

A

Promote LTD and reduce LTP

Physl (94 decks)

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