Calcium channels and short-term synaptic plasticity.

ABSTRACT

Voltage-gated Ca(2+) 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 Ca(2+) entry, placing the Ca(2+) 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 Ca(2+) entry for neurotransmission in the central nervous system. They are tightly regulated by Ca(2+), calmodulin, and related Ca(2+) 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.