Extracellular Calcium Depletion in Synaptic Transmission

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Abstract
Regulation of Ca2+ homeostasis in the extracellular space plays an important role in neuronal function. Several modeling studies and recent measurements have demonstrated that modest action potential or synaptic activity can result in a significant reduction in extracellular calcium ([Ca]o2+). Changes in [Ca]o 2+ can regulate intracellular signaling enzymes, such as Ca2+/calmodulin–dependent protein kinase II, and influence neuronal function at synaptic and nonsynaptic sites. The change in [Ca]o 2+ can affect several types of ion channels and neurotransmitter receptors and activate a Ca2+-sensitive receptor in neuronal membranes. Depletion of [Ca]o 2+ may function as an activity-dependent extracellular messenger that regulates nervous system function during development, learning, and disease.