Abstract
Presynaptic Ca2+ entry occurs through voltage-gated Ca2+ (CaV) channels which are activated by membrane depolarization. Depolarization accompanies neuronal firing and elevation of Ca2+ triggers neurotransmitter release from synaptic vesicles. For synchronization of efficient neurotransmitter release, synaptic vesicles are targeted by presynaptic Ca2+ channels forming a large signaling complex in the active zone. The presynaptic CaV2 channel gene family (comprising CaV2.1, CaV2.2, and CaV2.3 isoforms) encode the pore-forming α1 subunit. The cytoplasmic regions are responsible for channel modulation by interacting with regulatory proteins. This article overviews modulation of the activity of CaV2.1 and CaV2.2 channels in the control of synaptic strength and presynaptic plasticity.
Highlights
Presynaptic Ca2+ entry into the active zone (AZ) occurs through voltage-gated Ca2+ (CaV) channels which are activated membrane depolarization and triggers synchronous neurotransmitter release from synaptic vesicles (SVs)
To understand the physiological role of Ca2+ channel modulation in the regulation of synaptic transmission, a model synapse formed between sympathetic, superior cervical ganglion (SCG) neurons in culture was employed for functional study of channel interaction with G proteins, SNARE proteins, and Ca2+-binding proteins which sense residual Ca2+ in the AZ after the arrival of an action potential (AP)
Modulation of presynaptic Ca2+ channels has a powerful influence on synaptic transmission
Summary
Presynaptic Ca2+ entry into the active zone (AZ) occurs through voltage-gated Ca2+ (CaV) channels which are activated membrane depolarization and triggers synchronous neurotransmitter release from synaptic vesicles (SVs). Following a brief overview of Ca2+ channel structure/function, this article reviews the molecular and cellular mechanisms that modulate the activity of presynaptic Ca2+ channels in the regulation of neurotransmitter release and in the induction of short-term synaptic plasticity. To understand the physiological role of Ca2+ channel modulation in the regulation of synaptic transmission, a model synapse formed between sympathetic, superior cervical ganglion (SCG) neurons in culture was employed for functional study of channel interaction with G proteins, SNARE proteins, and Ca2+-binding proteins which sense residual Ca2+ in the AZ after the arrival of an action potential (AP). T(ha)e Tsuhbeusnuitbcuonmitpcoosmitipoonsaitniodnstarnucdtusrtreuocftuhirgeho-f hvigohlt-avgoelt-aagctei-vaactteivdatCead2+Ccah2+ancnhealns.neTlhs.eTchreyocr-EyoM-EsMtrustcrtuucrteuroef otfhteherarbabbibtitvvooltlataggee-g-gaateteddCCaa22++cchhaannnneel l CCaavv11.1.1ccoommpplelexxaattaannoommiinnaallrreessoolluuttiioonn ooff 44..22.
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