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Opioids act through two pathways to influence the activity of nerve cells. In one pathway, voltage-gated...

Question:

Opioids act through two pathways to influence the activity of nerve cells. In one pathway, voltage-gated Ca2+ channels in the

Opioids act through two pathways to influence the activity of nerve cells. In one pathway, voltage-gated Ca2+ channels in the nerve terminals are prevented from opening. Based on your understanding of the role of voltage-gated Cat in the pre- synaptic nerve cell, the effect of this would be to Answers A-D A prevent the influx of Ca2*, resulting in sustained release of neurotransmitter from the pre-synaptic cell. B to increase the duration of the action potential. o C prevent the influx of Ca2*, inhibiting secretion of neurotransmitters by fusion of secretory vesicles with the cell membrane. D prevent the influx of Ca2+, preventing the nerve cell from repolarizing. o

Answers

Option A : Prevent the influx cCa2+, resulting in sustained release of neurotransmitter from the pre-synaptic cell

Ca2+ influx through voltage-gated Ca2+ (Cav) channels at presynaptic nerve terminals is an essential step in neurotransmission and plays a crucial role in short-term synaptic plasticity. Multiple mechanisms modulate the function of presynaptic Cav2 channels and thereby regulate synaptic transmission

Voltage-gated Ca2+ channels in presynaptic nerve terminals initiate neurotransmitter release in response to depolarization by action potentials from the nerve axon. The strength of synaptic transmission is dependent on the 3rd to 4th power of Ca2+ entry, placing the Ca2+ channels in a unique position for regulation of synaptic strength. Short-term synaptic plasticity regulates strength of neurotransmission through facilitation and depression on the millisecond time scale and plays a key role in encoding information in the nervous system. CaV2.1 channels are the major source of Ca2+ entry for neurotransmission in the central nervous system.

They are tightly regulated by Ca2+, calmodulin, and related Ca2+ sensor proteins, which cause facilitation and inactivation of channel activity. Emerging evidence reviewed here points to this mode of regulation of CaV2.1 channels as a major contributor to short-term synaptic plasticity of neurotransmission and its diversity among synapses.

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