Signal-transduction pathways causing slow synaptic excitation in guinea pig myenteric AH neurons Bertrand, P. P en_US Galligan, J. J. en_US 2021-11-25T13:35:22Z 2021-11-25T13:35:22Z 1995 en_US
dc.description.abstract Intracellular recordings were obtained from myenteric AH neurons of guinea pig ileum in vitro. Slow excitatory synaptic responses associated with decreased potassium conductance (gK), inhibition of the spike afterhyperpolarization current (AHC), and increased chloride conductance (gCl) were mimicked by senktide, a neurokinin3 receptor agonist. Intracellular guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S) decreased gK and increased gCl irreversibly after nerve stimulation or senktide application. Myenteric neurons in pertussis toxin (PTX)- treated tissues responded normally to senktide and nerve stimulation. Forskolin and phorbol 12,13-dibutyrate (PDBu) inhibited gK and the AHC but did not activate gCl. The AHC was not reduced by subthreshold concentrations of forskolin (10 nM) or PDBu (3 nM) alone but was inhibited by forskolin and PDBu applied together. Inhibitors of phospholipase C (D-609) or protein kinases (staurosporine) reduced slow synaptic and senktide responses. The protein phosphatase inhibitor, calyculin A, caused an inward current, a decrease in gK, and AHC inhibition but did not activate gCl. We conclude that slow excitatory synaptic responses are mediated by PTX-insensitive G proteins and activation of phospholipase C and protein kinases. Forskolin and PDBu activate pathways that inhibit gK. The mechanisms for activation of gCl are unknown. en_US
dc.description.uri en_US
dc.identifier.issn 0193-1857 en_US
dc.language English
dc.language.iso EN en_US
dc.rights CC BY-NC-ND 3.0 en_US
dc.rights.uri en_US
dc.source Legacy MARC en_US
dc.title Signal-transduction pathways causing slow synaptic excitation in guinea pig myenteric AH neurons en_US
dc.type Journal Article en
dcterms.accessRights metadata only access
dspace.entity.type Publication en_US
unsw.relation.faculty Medicine & Health
unsw.relation.ispartofissue 5 en_US
unsw.relation.ispartofjournal American Journal of Physiology en_US
unsw.relation.ispartofpagefrompageto G710-G720 en_US
unsw.relation.ispartofvolume 269 en_US
unsw.relation.originalPublicationAffiliation Bertrand, P. P, Medical Sciences, Faculty of Medicine, UNSW en_US
unsw.relation.originalPublicationAffiliation Galligan, J. J. en_US School of Medical Sciences *
Resource type