Abstract
Voltage-gated calcium channels are the principal conduits for depolarization-mediated Ca2+ entry into excitable cells. In this review, the biophysical properties of the relevant members of this family of channels, those that are present in presynaptic terminals, will be discussed in relation to their function in mediating neurotransmitter release. Voltage-gated calcium channels have properties that ensure they are specialized for particular roles, for example, differences in their activation voltage threshold, their various kinetic properties, and their voltage-dependence of inactivation. All these attributes play into the ability of the various voltage-gated calcium channels to participate in different patterns of presynaptic vesicular release. These include synaptic transmission resulting from single action potentials, and longer-term changes mediated by bursts or trains of action potentials, as well as release resulting from graded changes in membrane potential in specialized sensory synapses.
Highlights
Voltage-gated calcium (CaV) channels are well understood to function as the route for Ca2þ entry into cells, excitable cells, in response to depolarization
All these attributes play into the ability of the various voltage-gated calcium channels to participate in different patterns of presynaptic vesicular release
These include synaptic transmission resulting from single action potentials, and longer-term changes mediated by bursts or trains of action potentials, as well as release resulting from graded changes in membrane potential in specialized sensory synapses
Summary
Voltage-gated calcium (CaV) channels are well understood to function as the route for Ca2þ entry into cells, excitable cells, in response to depolarization. CaV3 channels do not normally supply significant amounts of Ca2þ for neurotransmitter release resulting from action potentials arriving at the terminal, their availability can be affected by the interplay of other channels such as HCN channels and Ca2þ-activated Kþ channels, which affect membrane potential.[50] Functional HCN1 channels are present on particular glutamatergic synaptic terminals, for example onto entorhinal cortical layer III pyramidal neurons, where they depolarize the membrane potential and reduce neurotransmitter release These effects at least partly result from reduced availability of CaV3.2 channels.[50] CaV3 channels were found to play an important part in asynchronous dendrodendritic release of glutamate from olfactory bulb mitral cells.[107] In another study GABA release from interneurons could be promoted by activation of presynaptic nicotinic receptors and subsequent activation of presynaptic CaV3.1 channels, together with release of Ca2þ from ryanodinesensitive intracellular stores.[108] there is evidence from numerous studies for a variety of presynaptic roles for T-type channels
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