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Mediation by Protein Kinases C and A of G(o)-Linked Slow Responses of Enteric Neurons to 5-HT
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Mediation by Protein Kinases C and A of G(o)-Linked Slow Responses of Enteric Neurons to 5-HT

Hui Pan, Hoau-Yan Wang, Eitan Friedman and Michael D. Gershon
The Journal of neuroscience, v 17(3), pp 1011-1024
01 Feb 1997
PMID: 8994056
url
https://doi.org/10.1523/jneurosci.17-03-01011.1997View
Published, Version of Record (VoR)Maybe Open Access (Publisher Bronze) Open
url
https://doi.org/10.1523/JNEUROSCI.17-03-01011.1997View
Published, Version of Record (VoR) Open

Abstract

Articles
5-HT activates the peristaltic reflex and is the neurotransmitter of a subset of myenteric interneurons. Hyperpolarizing afterpotential (AH)/type 2 neurons respond to 5-HT with a long-lived depolarization that is caused by the inhibition of a Ca(2+)-activated K(+) conductance (gK(Ca)). This effect is mediated by a G-protein-coupled receptor, 5-HT(1P). 5-HT(1P) agonists specifically activate Gα(o), the immunoreactivity of which was found to be highly abundant and membrane-associated in almost all enteric neurons. Responses of hyperpolarizing AH/type 2 neurons to 5-HT were inhibited by intracellular injection of GDPβS or anti-Gα(o) Fab fragments but were potentiated and prolonged by intracellular GTPγS. Responses to 5-HT were antagonized by pertussis toxin, downregulation of protein kinase C (PKC) and inhibitors of phosphatidylcholine phospholipase C (PC-PLC), PKC (including pseudosubstrate peptides, chelerythrine, and the α/β isoform-specific inhibitor G(ö) 6976), protein kinase A (PKA), and adenylate cyclase. Responses to 5-HT were mimicked by activators of PKC, and 5-HT induced a concentration-dependent increase in the membrane-associated PKC activity in isolated myenteric ganglia. Immunocytochemical studies suggested that the most abundant isoforms of PKC in enteric neurons are α and δ. These data suggest that signal transduction of the 5-HT(1P)-mediated slow response to 5-HT involves activation of PC-PLC by Gα(o) to liberate diacylglycerol, which stimulates PKC (most likely α). PKC probably activates adenylate cyclase, which through cAMP, activates PKA. Activation of both PKA and PKC lead to closure of gK(Ca).

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Neurosciences
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