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