Neuronal Ca2+ signalling at rest and during spontaneous neurotransmission

Abstract

Action potential driven neuronal signaling drives several electrical and biochemical processes in the nervous system. However, neurons can maintain synaptic communication and signaling under resting conditions independent of activity. Importantly, these processes are regulated by Ca²⁺ signals that occur at rest. Several studies have suggested that opening of voltage‐gated Ca²⁺ channels near resting membrane potentials, activation of NMDA receptors in the absence of depolarization or Ca²⁺ release from intracellular stores can drive neurotransmitter release as well as subsequent signalling in the absence of action potentials. Interestingly, recent studies have demonstrated that manipulation of resting neuronal Ca²⁺ signalling yielded pronounced homeostatic synaptic plasticity suggesting a critical role for this resting form of signalling in regulation of synaptic efficacy and neuronal homeostasis. Given their robust impact on synaptic efficacy and neuronal signalling, neuronal resting Ca²⁺ signals warrant further mechanistic analysis that include the potential role of store‐operated Ca²⁺ entry in these processes.

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