| Sign In to gain access to subscriptions and/or personal tools. |
DOI: 10.1177/1073858403259440 Extracellular Calcium Depletion in Synaptic Transmission
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+/calmodulindependent 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
This article has been cited by other articles:
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||




