Martín Herranz, RicardoBartolomé-Martín, DavidTorres Molina, Magdalena IsabelSánchez-Prieto Borja, José2024-01-302024-01-302011-020022-304210.1111/j.1471-4159.2010.07134.xhttps://hdl.handle.net/20.500.14352/96435We 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 Ca2+ channels, because phorbol ester and mGlu7 receptor-mediated release potentiation are absent in nerve terminals from mice lacking N-type Ca2+ channels. In addition, phorbol esters but not mGlu7 receptors potentiate release at nerve terminals with P/Q-type Ca2+ channels, although only under restricted conditions of Ca2+ influx. The differential effect of phorbol esters at nerve terminals with either N- or P/Q-type Ca2+ channels seems to be unrelated to the type Munc13 isoform expressed, and it is more likely dependent on other properties of the release machinery.engAttribution-NonCommercial-NoDerivatives 4.0 Internationalhttp://creativecommons.org/licenses/by-nc-nd/4.0/journal article1471-4159https://onlinelibrary.wiley.com/doi/10.1111/j.1471-4159.2010.07134.x21143597open access612.8636.09Glutamate release potentiationmGluR7Munc13-1Munc13-2Nerve terminal lacking N-type Ca2+ channelsN-type Ca2+ channelsP/Q-type Ca2+ channelsPhorbol estersNeurociencias (Biológicas)Veterinaria2490 Neurociencias3109 Ciencias Veterinarias