Neuron
ArticleVIP inhibits N-type Ca2+ channels of sympathetic neurons via a pertussis toxin-insensitive but cholera toxin-sensitive pathway
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2021, Pharmacological ResearchCitation Excerpt :The transduction mechanisms contributing to the VPAC receptor-mediated rise in [Ca2+]i include both Gαi and Gαq coupled pathways, with the Gαi contribution estimated to account for ∼ 40 % of the total [Ca2+]i response in VPAC receptor stable cell lines (human and rat receptors) [80]; This is essentially different from the PAC1 receptor-mediated stimulation of [Ca2+]i, which appears to be exclusively mediated via Gαq and in some cases operated by L-type voltage-gated calcium channels (VGCCs) [81,82]. Interestingly, both VIP and PACAP can control neuronal [Ca2+]i by inhibiting L-, N- and P/Q-type Ca2+ channels in parasympathetic neurons in a voltage-independent manner [83]; this action was Gs-dependent, but Gi-independent, concerning the inhibitory effect operated on N-type channels in the rat [84]. Remarkably, the expression patterns of VIP receptor subtypes in the CNS are very distinct.
Regulation of Ca<inf>V</inf>2 calcium channels by G protein coupled receptors
2013, Biochimica et Biophysica Acta - BiomembranesCitation Excerpt :For example, PKC has been implicated in the inhibition of N-type ICa in chick sensory neurons [247,248]. In frog and mammalian neurons PKC can also potentiate ICa, might target multiple phosphorylation sites with opposing actions, antagonize Gβγ mediated inhibition, or modulate channel trafficking (see Sections 8, 9) [155,180,181,249,250]. It was also reported that rapid activation of a tyrosine kinase by GABAB receptors resulted in voltage-independent inhibition of N-type ICa in chick sensory neurons [251].
GPCR mediated regulation of synaptic transmission
2012, Progress in NeurobiologyCitation Excerpt :Subsequent studies over the next 20 years have implicated primarily Gi/o-coupled GPCRs in this regulation as muscarinic, opioid, dopamine, and many other Gi/o-coupled receptors all have the propensity to exert negative control over calcium currents and exhibit sensitivity to pertussis toxin (Bean, 1989; Boland and Bean, 1993; Elmslie, 1992; Golard and Siegelbaum, 1993; Kasai and Aosaki, 1989). However, it should be noted that modulation of VDCC may not occur solely through the actions of Gi/o-coupled GPCRs as activation of Gs and Gz-coupled G proteins has also been shown to mediate voltage-dependent inhibition of N-type calcium channels (Zhu and Ikeda, 1994). Whether this reflects a ubiquitous mechanism of regulation remains unclear, however, it is apparent that inhibition of calcium channels by GPCRs is widespread and an important regulatory factor mediating control of neurotransmitter release.