AKAP79/150 signal complexes in G-protein modulation of neuronal ion channels.

ABSTRACT: Voltage-gated M-type (KCNQ) K+ channels play critical roles in regulation of neuronal excitability. Previous work showed A-kinase-anchoring protein (AKAP)79/150-mediated protein kinase C (PKC) phosphorylation of M channels to be involved in M current (I(M)) suppression by muscarinic M1, but not bradykinin B2, receptors. In this study, we first explored whether purinergic and angiotensin suppression of I(M) in superior cervical ganglion (SCG) sympathetic neurons involves AKAP79/150. Transfection into rat SCG neurons of ΔA-AKAP79, which lacks the A domain necessary for PKC binding, or the absence of AKAP150 in AKAP150(-/-) mice, did not affect I(M) suppression by purinergic agonist or by bradykinin, but reduced I(M) suppression by muscarinic agonist and angiotensin II. Transfection of AKAP79

SUBMITTER: Zhang J 

PROVIDER: S-EPMC3114554 | biostudies-literature | 2011 May

REPOSITORIES: biostudies-literature