1. Which statement about the plasticity of synapses in the mammalian CNS is false?
A. calcium ions play a central role in at least some forms of synaptic plasticity
B. the efficacy of synapses can be adjusted by modulating the amount of neurotransmitter that is released
C. a variety of molecular mechanisms are involved in the different forms of synaptic plasticity
D. the hallmark of both short-term and long-term synaptic plasticity is that they always increase in the strength of synaptic connections
E. changes in synaptic efficacy can occur over time scales ranging from milliseconds to years
2. after firing a short burst of action potentials in an axon, researchers observe a larger EPSP in the post synaptic cell, and this effect seems to last a few tens to milliseconds. This is most likely due to the presynaptic terminal having
A. reduced sodium
B. lowered calcium
C. extra calcium
D. extra magnesium
E. extra sodium
3. Which mechanism would be a plausible explanation for synaptic depression?
A. inhibition of postsynaptic calcium channels
B. activation of presynaptic potassium channels
C. depletion of docked synaptic vesicles in the presynaptic terminal
D. enhancement of presynaptic sodium currents
E. Faster replenishment of vesicles to the reserve pool
1) synaptic plasticity is an ability of synapse to modify its strength according to its activity.
Molecular mechanisms involves NMDA and AMPA receptors for glutamate.
Strong depolarization→Magnesium ions completely displace and block NMDA→↑ Calcium ions→ long term potentiation
Weak depolarization→↓ magnesium ions displaced and incompletely block NMDA→↓ Calcium ions→ long term depression.
false statement-d
2)firing of short bursts accumulate extra calcium in pre synaptic membrane. The Calcium from next depolarization gets added to the previous pool and give an augmented response which is a larger EPSP
Answer- c- extra calcium.
3) synaptic depression is most likely linked to depletion of release ready pool of synaptic vesicles.
answer-c
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