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Synaptically activated Ca 2+ waves and NMDA spikes locally suppress voltage‐dependent Ca 2+ signalling in rat pyramidal cell dendrites
Author(s) -
Manita Satoshi,
Miyazaki Kenichi,
Ross William N.
Publication year - 2011
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2011.216564
Subject(s) - biophysics , nmda receptor , depolarization , tetanic stimulation , chemistry , hippocampal formation , synaptic plasticity , postsynaptic potential , pyramidal cell , neuroscience , neurotransmission , biology , biochemistry , receptor
Non‐Technical Summary Synaptically activated changes in dendritic [Ca 2+ ] i affect many important physiological processes including synaptic plasticity and gene expression. The location, magnitude and time course of these changes can determine which mechanisms are affected. Therefore, it is important to understand the processes that control and modulate these changes. One important source is Ca 2+ entering through voltage‐gated Ca 2+ channels opened by action potentials backpropagating over the dendrites (bAPs). Here we examine how [Ca 2+ ] i changes, caused by regenerative Ca 2+ release from internal stores (Ca 2+ waves) or by regenerative Ca 2+ entry through NMDA receptors (NMDA spikes), affect subsequent bAP‐evoked [Ca 2+ ] i changes. These large [Ca 2+ ] i increases suppressed the bAP signals in the regions where the preceding [Ca 2+ ] i increases were largest. The suppression was proportional to the magnitude of the large [Ca 2+ ] i change and was insensitive to kinase and phosphatase inhibitors, consistent with suppression due to Ca 2+ ‐dependent inhibition of Ca 2+ channels.