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A novel fast mechanism for GPCR-mediated signal transduction—control of neurotransmitter release

Reliable neuronal communication depends on accurate temporal correlation between the action potential and neurotransmitter release. Although a requirement for Ca(2+) in neurotransmitter release is amply documented, recent studies have shown that voltage-sensitive G protein–coupled receptors (GPCRs)...

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Detalles Bibliográficos
Autores principales: Kupchik, Yonatan M., Barchad-Avitzur, Ofra, Wess, Jürgen, Ben-Chaim, Yair, Parnas, Itzchak, Parnas, Hanna
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3019563/
https://www.ncbi.nlm.nih.gov/pubmed/21200029
http://dx.doi.org/10.1083/jcb.201007053
Descripción
Sumario:Reliable neuronal communication depends on accurate temporal correlation between the action potential and neurotransmitter release. Although a requirement for Ca(2+) in neurotransmitter release is amply documented, recent studies have shown that voltage-sensitive G protein–coupled receptors (GPCRs) are also involved in this process. However, how slow-acting GPCRs control fast neurotransmitter release is an unsolved question. Here we examine whether the recently discovered fast depolarization-induced charge movement in the M(2)-muscarinic receptor (M(2)R) is responsible for M(2)R-mediated control of acetylcholine release. We show that inhibition of the M(2)R charge movement in Xenopus oocytes correlated well with inhibition of acetylcholine release at the mouse neuromuscular junction. Our results suggest that, in addition to Ca(2+) influx, charge movement in GPCRs is also necessary for release control.