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Extracellular Calcium Depletion in Synaptic Transmission

R. Douglas Fields

National Institutes of Health National Institute for Child and Human Development Section on Nervous System Development and Plasticity fields{at}helix.nih.gov

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.

Key Words: Cadherin • Calcium-sensitive receptor • CaMKII • Extracellular calcium • Long-term potentiation • Synaptic plasticity

The Neuroscientist, Vol. 10, No. 1, 12-17 (2004)
DOI: 10.1177/1073858403259440


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