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Non‐additive potentiation of glutamate release by phorbol esters and metabotropic mGlu7 receptor in cerebrocortical nerve terminals
Author(s) -
Martín Ricardo,
BartoloméMartín David,
Torres Magdalena,
SánchezPrieto José
Publication year - 2011
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2010.07134.x
Subject(s) - metabotropic glutamate receptor , long term potentiation , metabotropic glutamate receptor 6 , chemistry , metabotropic glutamate receptor 1 , metabotropic glutamate receptor 7 , metabotropic receptor , microbiology and biotechnology , pertussis toxin , metabotropic glutamate receptor 5 , protein kinase c , glutamate receptor , biochemistry , receptor , g protein , biology , signal transduction
J. Neurochem. (2011) 116 , 476–485. Abstract We recently showed that prolonged activation of metabotropic glutamate receptor 7 (mGlu7) potentiates glutamate release. This signalling involves phospholipase C activation via a pertussis toxin insensitive G protein and the subsequent hydrolysis of phosphatidylinositol (4,5)‐bisphosphate. Release potentiation is independent of protein kinase C activation but it is dependent on the downstream release machinery, as reflected by the concomitant translocation of active zone Munc13‐1 protein from the soluble to particulate fractions. Here we show that phorbol ester and mGlu7 receptor‐dependent facilitation of neurotransmitter release is not additive, suggesting they share a common signalling mechanism. However, release potentiation is restricted to release sites that express N‐type Ca 2+ channels, because phorbol ester and mGlu7 receptor‐mediated release potentiation are absent in nerve terminals from mice lacking N‐type Ca 2+ channels. In addition, phorbol esters but not mGlu7 receptors potentiate release at nerve terminals with P/Q‐type Ca 2+ channels, although only under restricted conditions of Ca 2+ influx. The differential effect of phorbol esters at nerve terminals with either N‐ or P/Q‐type Ca 2+ channels seems to be unrelated to the type Munc13 isoform expressed, and it is more likely dependent on other properties of the release machinery.