| http://purl.uniprot.org/citations/23174341 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/23174341 | http://www.w3.org/2000/01/rdf-schema#comment | "Calcium channels that mediate glutamate release (N-type and P/Q-type) are expressed in distinct populations of cerebrocortical nerve terminals in adult mice. mGlu7 receptors are exclusively expressed in nerve terminals containing N-type Ca(2+) channels, which are less tightly coupled to glutamate release than P/Q-type Ca(2+) channels. We recently reported that in addition to inhibit, mGlu7 receptors can also potentiate glutamate release via phosphatidyl inositol (4,5)-bisphosphate hydrolysis and activation of the non-kinase diacylglycerol binding protein Munc13-1, a protein that primes synaptic vesicles for exocytosis. Here, we assessed whether mGlu7 receptor-mediated potentiation of glutamate release is restricted to nerve terminals expressing N-type Ca(2+) channels to compensate for their weak coupling to release. In the hippocampus, mGlu7 receptors are expressed both in nerve terminals containing N-type Ca(2+) channels and in nerve terminals containing P/Q-type Ca(2+) channels. When analyzed, we observed potentiation of mGlu7 receptor mediated release in wild type hippocampal nerve terminals at physiological (1.3 mM) and low (0.1 mM) concentrations of external Ca(2+). By contrast, in nerve terminals from mice lacking the α1B subunit of N-type channels (Ca(v)2.2), in which evoked release is mediated by P/Q-type channels only, no release potentiation was observed at 1.3 mM Ca(2+). We conclude that release potentiation at 1.3 mM [Ca(2+)](e) occurs in nerve terminals expressing N-type channels, whereas that which occurs at low 0.1 mM [Ca(2+)](e) represents the release from nerve terminals containing P/Q-type Ca(2+) channels. Although, mGlu7 receptor mediated potentiation is independent of Ca(2+) channel activity, as it was induced by the Ca(2+) ionophore ionomycin, release potentiation is influenced by the Ca(2+) channel type and/or the associated release machinery."xsd:string |
| http://purl.uniprot.org/citations/23174341 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.neuropharm.2012.10.032"xsd:string |
| http://purl.uniprot.org/citations/23174341 | http://purl.uniprot.org/core/author | "Torres M."xsd:string |
| http://purl.uniprot.org/citations/23174341 | http://purl.uniprot.org/core/author | "Bartolome-Martin D."xsd:string |
| http://purl.uniprot.org/citations/23174341 | http://purl.uniprot.org/core/author | "Sanchez-Prieto J."xsd:string |
| http://purl.uniprot.org/citations/23174341 | http://purl.uniprot.org/core/author | "Ferrero J.J."xsd:string |
| http://purl.uniprot.org/citations/23174341 | http://purl.uniprot.org/core/date | "2013"xsd:gYear |
| http://purl.uniprot.org/citations/23174341 | http://purl.uniprot.org/core/name | "Neuropharmacology"xsd:string |
| http://purl.uniprot.org/citations/23174341 | http://purl.uniprot.org/core/pages | "213-222"xsd:string |
| http://purl.uniprot.org/citations/23174341 | http://purl.uniprot.org/core/title | "Potentiation of mGlu7 receptor-mediated glutamate release at nerve terminals containing N and P/Q type Ca2+ channels."xsd:string |
| http://purl.uniprot.org/citations/23174341 | http://purl.uniprot.org/core/volume | "67"xsd:string |
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