Action potential driven neuronal signalling drives several electrical and biochemical processes in the nervous system. However, neurons can maintain synaptic communication and signalling under resting conditions independently of activity. Importantly, these processes are regulated by Ca 2+ signals that occur at rest. Several studies have suggested that opening of voltage-gated Ca 2+ channels near resting membrane potentials, activation of NMDA receptors in the absence of depolarization or Ca 2+ 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 Ca 2+ 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 Ca 2+ signals warrant further mechanistic analysis that includes the potential role of store-operated Ca 2+ entry in these processes. (Figure presented.).
- Ca stores
- Spontaneous neurotransmitter release
- store-operated Ca entry
- voltage gated Ca channel
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