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This Article Full Text Full Text (PDF) All Versions of this Article: 581/2/787    most recent jphysiol.2007.128082v2 jphysiol.2007.128082v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Krauter, E. M. Articles by Mawe, G. M. Search for Related Content PubMed PubMed Citation Articles by Krauter, E. M. Articles by Mawe, G. M. Related Collections Alimentary

¹ Department of Anatomy and Neurobiology, The University of Vermont College of Medicine, Burlington, VT, USA
² Department of Physiology and Biophysics, University of Calgary, Calgary, Alberta, Canada

The purpose of this study was to investigate the pre- and postsynaptic mechanisms that contribute to synaptic facilitation in the myenteric plexus of the trinitrobenzene sulphonic acid-inflamed guinea-pig distal colon. Intracellular recordings of evoked fast excitatory postsynaptic potentials (fEPSPs) in myenteric S neurons were evaluated, and the density of synaptic terminals was morphometrically analysed by transmission electron microscopy. In inflamed tissue, fEPSPs were reduced to control levels by the protein kinase A (PKA) inhibitor, H89, but H89 did not affect the fEPSPs in control tissue. This PKA activation in inflamed tissue did not appear to involve 5-HT₄ receptors because the antagonist/inverse agonist, GR 125487, caused comparable decreases of fEPSPs in both tissues. Inhibition of BK channels with iberiotoxin did not alter the fEPSPs in inflamed tissue, but increased the fEPSPs in control tissue to the amplitude detected in inflamed tissue. During trains of stimuli, run-down of EPSPs was less extensive in inflamed tissue and there was a significant increase in the paired pulse ratio. Depolarizations in response to exogenous neurotransmitters were not altered in inflamed tissue. These inflammation-induced changes were not accompanied by alterations in the pharmacological profile of EPSPs, and no changes in synaptic density were detected by electron microscopy. Collectively, these data indicate that synaptic facilitation in the inflamed myenteric plexus involves a presynaptic increase in PKA activity, possibly involving an inhibition of BK channels, and an increase in the readily releasable pool of synaptic vesicles.

(Received 10 January 2007; accepted after revision 15 March 2007; first published online 15 March 2007)
Corresponding author G. M. Mawe: Department of Anatomy and Neurobiology, Given D403A, University of Vermont, Burlington, VT 05405, USA. Email gary.mawe{at}uvm.edu

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