Abstract
Neuronal voltage-gated calcium channels have evolved as one of the most important players for calcium entry into presynaptic endings responsible for the release of neurotransmitters. In turn, and to fine-tune synaptic activity and neuronal communication, numerous neurotransmitters exert a potent negative feedback over the calcium signal provided by G protein–coupled receptors. This regulation pathway of physiologic importance is also extensively exploited for therapeutic purposes, for instance in the treatment of neuropathic pain by morphine and other μ-opioid receptor agonists. However, despite more than three decades of intensive research, important questions remain unsolved regarding the molecular and cellular mechanisms of direct G protein inhibition of voltage-gated calcium channels. In this study, we revisit this particular regulation and explore new considerations.
Footnotes
- Received September 18, 2014.
- Accepted December 30, 2014.
The work in N.W.’s laboratory was supported by the Czech Science Foundation [Grant 15-13556S] and the Institute of Organic Chemistry and Biochemistry (IOCB). J.P. is supported by a postdoctoral fellowship from IOCB.
- Copyright © 2015 by The American Society for Pharmacology and Experimental Therapeutics
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