Abstract
The Cav2 family of voltage-gated calcium channels consists of 3 main subtypes (Cav2.1, Cav2.2 and Cav2.3), defined by their (α1 subunit (α12.1, α12.2 and α12.3, respectively; also known as α1A,α1B and αE). The use of selective peptide toxins has allowed the association of Cav2.1, 2.2 and 2.3 with P- or Q-, N-, and B-type calcium currents, respectively (Catterall, 2000; Ertel et al., 2000; Jarvis and Zamponi, 2001). These currents are found almost exclusively in the CNS, PNS and neuroendocrine cells and constitute the predominant forms of presynaptic voltage-gated calcium current. Presynaptic action potentials cause channel opening, and neurotransmitter release is steeply dependent upon the subsequent calcium entry (Meir et al., 1999; Sabatini and Regehr, 1999). Presynaptic calcium entry is modulated by many types of G-protein coupled receptors (GPCRs), and studies with agonists for these receptors indicate that modulation of Cav2 channels is a widespread and highly efficacious means of regulating neurotransmission. In this review, we describe the prospects for targeting Cav2 channels with novel therapeutic agents.
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