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Publication : A novel fast mechanism for GPCR-mediated signal transduction--control of neurotransmitter release.

First Author  Kupchik YM Year  2011
Journal  J Cell Biol Volume  192
Issue  1 Pages  137-51
PubMed ID  21200029 Mgi Jnum  J:167982
Mgi Id  MGI:4881570 Doi  10.1083/jcb.201007053
Citation  Kupchik YM, et al. (2011) A novel fast mechanism for GPCR-mediated signal transduction--control of neurotransmitter release. J Cell Biol 192(1):137-51
abstractText  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.
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