G protein βγ subunits inhibit TRPM3 ion channels in sensory neurons, 2017, Quallan, Bevan et al

Andy · May 28, 2019

Two of the authors of this paper are presenting at the IiME conference this year, Stuart Bevan on pain and ME and David Andersson on fibromyalgia.

Abstract

Transient receptor potential (TRP) ion channels in peripheral sensory neurons are functionally regulated by hydrolysis of the phosphoinositide PI(4,5)P2 and changes in the level of protein kinase mediated phosphorylation following activation of various G protein coupled receptors. We now show that the activity of TRPM3 expressed in mouse dorsal root ganglion (DRG) neurons is inhibited by agonists of the Gi-coupled µ opioid, GABA-B and NPY receptors. These agonist effects are mediated by direct inhibition of TRPM3 by Gβγ subunits, rather than by a canonical cAMP mediated mechanism. The activity of TRPM3 in DRG neurons is also negatively modulated by tonic, constitutive GPCR activity as TRPM3 responses can be potentiated by GPCR inverse agonists. GPCR regulation of TRPM3 is also seen in vivo where Gi/o GPCRs agonists inhibited and inverse agonists potentiated TRPM3 mediated nociceptive behavioural responses.
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Open access at https://elifesciences.org/articles/26138

wastwater · May 28, 2019

PAX6 regulates TRPM3
https://www.researchgate.net/public...s_and_transcriptional_control_of_Trpm3miR-204

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G protein βγ subunits inhibit TRPM3 ion channels in sensory neurons, 2017, Quallan, Bevan et al

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G protein βγ subunits inhibit TRPM3 ion channels in sensory neurons, 2017, Quallan, Bevan et al

Andy Committee Member

wastwater Senior Member (Voting Rights)

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