IndraLab

Statements


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reach
"Neuronal voltage-gated N-type calcium channels (Cav2.2) are inhibited by activation of G protein-coupled opioid receptors (ORs)."

reach
"Finally, since N-, P/Q- and R-type calcium currents can be inhibited by activation of GPCRs that are linked to G (for a review, see [20]), we tested if (S)-LCM affects G-protein inhibition of CaV2.2, which can be relieved by depolarization."

sparser
"Finally, since N-, P/Q- and R-type calcium currents can be inhibited by activation of GPCRs that are linked to G i/o (for a review, see [ xref ]), we tested if ( S )-LCM affects G-protein inhibition of CaV2.2, which can be relieved by depolarization. ( S )-LCM did not affect the ratio of currents between the pulses ( xref ), ruling out involvement of G-proteins in its regulation of CaV2.2."

reach
"G-protein coupled receptors inhibit Cav2.2 N-type Ca2+ channels by a fast, voltage-dependent pathway mediated by Gαi/Gβγ and a slow, voltage-independent pathway mediated by Gαq-dependent reductions in phosphatidylinositol 4,5-bisphosphate (PIP2) or increases in arachidonic acid."

reach
"Indeed, it has been shown G protein inhibition of Cav2.2 channels triggered by activation of μ-opioid receptors (MORs) is altered in channels containing exon 37a [28, 29], such that there is an increase in tyrosine kinase-mediated voltage-independent inhibition and less classical voltage-dependent modulation that involves direct Gβγ interactions with the channel [30–33]."

sparser
"Indeed, it has been shown G protein inhibition of Cav2.2 channels triggered by activation of μ-opioid receptors (MORs) is altered in channels containing exon 37a [ xref , xref ], such that there is an increase in tyrosine kinase-mediated voltage-independent inhibition and less classical voltage-dependent modulation that involves direct Gβγ interactions with the channel [ xref – xref ]."