Extracellular Calcium Depletion in Synaptic Transmission  

Oleh:

Cohen, Jonathan E. ; Fields, R. Douglas

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: The Neuroscientist vol. 10 no. 1 (Feb. 2004), page 12–17.
Topik: Cadherin; Calcium-sensitive receptor; CaMKII; Extracellular calcium; Long-term potentiation; Synaptic plasticity
Fulltext: 12TN101.pdf (100.36KB)

Isi artikel

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]o2+ 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]o2+ can affect several types of ion channels and neurotransmitter receptors and activate a Ca2+-sensitive receptor in neuronal membranes. Depletion of [Ca]o2+ may function as an activity-dependent extracellular messenger that regulates nervous system function during development, learning, and disease.

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