Abstract
Neuronal voltage-gated calcium channels (VGCCs) serve complex yet essential physiological functions via their pivotal role in translating electrical signals into intracellular calcium elevations and associated downstream signalling pathways. There are a number of regulatory mechanisms to ensure a dynamic control of the number of channels embedded in the plasma membrane, whereas alteration of the surface expression of VGCCs has been linked to various disease conditions. Here, we provide an overview of the mechanisms that control the trafficking of VGCCs to and from the plasma membrane, and discuss their implication in pathophysiological conditions and their potential as therapeutic targets.
Highlights
Within neurons, calcium ions (Ca2 + ) are essential for regulating a myriad of cellular processes and physiological functions [1]
Voltage-gated calcium channels (VGCCs) are essential for the initiation of the Ca2 + signalling cascades that are triggered by membrane depolarizations
We have highlighted some of the elements of this machinery underlying the expression of VGCCs, and it is likely that a number of additional players have not yet been identified
Summary
Calcium ions (Ca2 + ) are essential for regulating a myriad of cellular processes and physiological functions [1]. We consider mechanisms that control the trafficking of VGCCs. We review the role of channel ancillary subunits and other interacting proteins in the expression of the channel.
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