Synaptic Plasticity

Question 1

What is Type I synapse?

Answer 1

Glutamatergic
Round synaptic vesicles
Large postsynaptic density

Question 2

What is Type II synapse?

Answer 2

GABAergic
Oval synaptic vesicles
Weak postysynaptic density

Question 3

T/F: AMPA receptors are able to provide enough depolarization to allow an action potential to fire

Answer 3

True

Question 4

What has to happen in order for NMDA receptors to control plasticity?

Answer 4

Binding of glutamate & glycine to LBD
Can only open once the membrane has been depolarized

Question 5

If the membrane is not depolarized why can’t NMDA receptors work?

Answer 5

Mg2 ion block channel pore
Voltage relieves Mg2 block

Question 6

Beginning with NMDA receptor activity & ending with cell death, what are the steps of excitotoxity?

Answer 6

– High levels of glutamate cause excessive NMDA receptor activity & excessive Ca to enter post synaptic
– High Ca generate free radicals & activate creation of nitric oxide
– Nitric oxide + Free radicals = peroxynitrite
– Peryoxynitrite causes DNA damage which causes apoptosis

Question 7

What can excessive extra synaptic Ca entry cause?

Answer 7

– Activate enzymes directly involve in breakdown of nucleus, membrane & mitochondria
– Activate nitric oxide synthase
– Inhibit function of mitochondria

Question 8

Beginning with NMDA receptor activity & ending with an increased likelihood of following an action potential, what are the steps of long term potentiation?

Answer 8

– High frequency (100Hz) glutamate release activates NMDA receptors
– Ca through NMDA receptors bind & activates calmodulin
– Ca + calmodulin activates adenylyl cyclase
– Adenyly cyclase leads to production of cAMP
– cAMP activates PKA
– PKA phosphorylation CREB
– P-CREB enhances expression of AMPA receptors
– Increased number AMPA receptor, which will increase current generated with the same glutamate exposure
– This will increase likelihood of an action potential firing