Voltage-gated calcium channels (CaV) are present in the membrane of most excitable cells and mediate calcium influx in response to depolarization. They regulate intracellular processes such as contraction, secretion, neurotransmission and gene expression.
Voltage-gated calcium channels (CaV) are present in the membrane of most excitable cells and mediate calcium influx in response to depolarization. They regulate processes such as muscle contraction, secretion, neurotransmission and gene expression.
CaV channels are formed from four or five distinct subunits: α1, α2, δ, β and γ. The transmembrane α1-subunit, for which there are 10 genes, is the largest subunit and incorporates the voltage sensor, conduction pore and gating apparatus. All other subunits have auxiliary roles and modulate the kinetics and current magnitude of the α1-subunit. The α2 and δ subunits are encoded by the same gene and are linked by a disulphide bond, with four α2/δ genes identified in humans. Similarly, four genes have been identified for the cytoplasmic β-subunit, and eight genes identified for the γ-subunit. Multiple genes for each subunit and alternative splicing of each gene generates a high degree of heterogeneity within CaV channels.
Using pharmacological and electrophysiological techniques, at least six types of voltage-gated channels have been identified, grouped into three families depending on their sensitivity to different blockers, single-channel conductance and voltage-dependence. CaV1.x are high-voltage-activated, dihydropyridine-sensitive channels (L-type), CaV2.x are high-voltage-activated, dihydropyridine-insensitive channels (N-, P/Q- and R-types) and CaV3.x are low-voltage-activated, low conductance channels (T-type).
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Major depressive disorder is characterized by depressed mood and a loss of interest and/or pleasure. Updated in 2015 this poster highlights presynaptic and postsynaptic targets for the potential treatment of major depressive disorder, as well as outlining the pharmacology of currently approved antidepressant drugs.
Recognition memory enables us to make judgements about whether or not we have encountered a particular stimulus before. This poster outlines the cellular mechanisms underlying recognition memory and its links to long-term depression, as well as the use of pharmacological intervention to assess the role of neurotransmitters in recognition memory.
Channel Type | L | T | N | P | Q | R |
---|---|---|---|---|---|---|
Conductance (pS) | 25 | 5-9 | ~ 20 | 9-19 | 16 | - |
Activation Threshold | High | Low | High | High | High | High |
Deactivation Rate | Fast | Slow | Fast | Fast | Fast | Fast |
Inactivation Rate | Slow | Fast | Moderate | Very Slow | Moderate | Fast |
Permeability | Ba2+ > Ca2+ | Ba2+ = Ca2+ | Ba2+ > Ca2+ | Ba2+ > Ca2+ | Ba2+ > Ca2+ | Ba2+ > Ca2+ |
Perez-Reyes and Schneider (1994) Calcium channels: structure, function, and classification. Drug Dev.Res. 33 295. Catterall (1995) Structure and function of voltage-gated ion channels. Ann.Rev.Biochem. 64 493.