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Synaptically activated ca2+ release from internal stores in CNS neurons.

Abstract

Synaptically activated postsynaptic [Ca2+]i increases occur through three main pathways: Ca2+ entry through voltage-gated Ca2+ channels, Ca2+ entry through ligand-gated channels, and Ca2+ release from internal stores. The first two pathways have been studied intensively; release from stores has been the subject of more recent investigations. Ca2+ release from stores in CNS neurons primarily occurs as a result of IP3 mobilized by activation of metabotropic glutamatergic and/or cholingergic receptors coupled to PLC. Ca2+ release is localized near spines in Purkinje cells and occurs as a wave in the primary apical dendrites of pyramidal cells in the hippocampus and cortex. The amplitude of the [Ca2+]i increase can reach several micromolar, significantly larger than the increase due to backpropagating spikes. The large amplitude, long duration, and unique location of the [Ca2+]i increases due to Ca2+ release from stores suggests that these increases can affect specific downstream signaling mechanisms in neurons.

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BibTeXRIS

William N Ross, Takeshi Nakamura, Shigeo Watanabe, Matthew Larkum, Nechama Lasser-Ross. 2005. Synaptically activated ca2+ release from internal stores in CNS neurons.. https://doi.org/10.1007/s10571-005-3060-0

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