Calcium Channels and Short-term Synaptic Plasticity

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 third to fourth power of Ca2+ entry, placing the Ca2+ channels in a unique position for regulation of synaptic strength. Short-term synaptic plasticity regulates the strength of neurotransmission through facilitation and depression on the millisecond time scale and plays a key role in encoding information in the nervous system. Ca(V)2.1 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 Ca(V)2.1 channels as a major contributor to short-term synaptic plasticity of neurotransmission and its diversity among synapses.