RT Journal Article
T1 Non-additive potentiation of glutamate release by phorbol esters and metabotropic mGlu7 receptor in cerebrocortical nerve terminals
A1 Martín Herranz, Ricardo
A1 Bartolomé-Martín, David
A1 Torres Molina, Magdalena Isabel
A1 Sánchez-Prieto Borja, José
AB 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 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.
PB Wiley
SN 0022-3042
YR 2011
FD 2011-02
LK https://hdl.handle.net/20.500.14352/96435
UL https://hdl.handle.net/20.500.14352/96435
LA eng
NO Ministerio de Educación y Ciencia (BFU2007-64154/BFI; BFU2010/16947)
NO Instituto de Salud Carlos III
NO Comunidad de Madrid (S-BIO-0179/2006)
DS Docta Complutense
RD 7 abr 2025