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Pacemaker shift in the gastric antrum of guinea‐pigs produced by excitatory vagal stimulation involves intramuscular interstitial cells
Author(s) -
Hirst G. D. S.,
Dickens E. J.,
Edwards F. R.
Publication year - 2002
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2002.018614
Subject(s) - excitatory postsynaptic potential , antrum , stimulation , interstitial cell of cajal , hyperpolarization (physics) , membrane potential , pacemaker potential , acetylcholine , apamin , inhibitory postsynaptic potential , vagus nerve , medicine , chemistry , endocrinology , neuroscience , biology , stomach , potassium channel , organic chemistry , nuclear magnetic resonance spectroscopy , immunohistochemistry
Intracellular recordings were made from isolated bundles of the circular muscle layer of guinea‐pig gastric antrum and the responses produced by stimulating intrinsic nerve fibres were examined. After abolishing the effects of stimulating inhibitory nerve terminals with apamin and l ‐nitroarginine (NOLA), transmural nerve stimulation often evoked a small amplitude excitatory junction potential (EJP) and invariably evoked a regenerative potential. Neurally evoked regenerative potentials had similar properties to those evoked in the same bundle by direct stimulation. EJPs and neurally evoked regenerative potentials were abolished by hyoscine suggesting that both resulted from the release of acetylcholine and activation of muscarinic receptors. Neurally evoked regenerative potentials, but not EJPs, were abolished by membrane hyperpolarization, caffeine and chloride channel blockers. In the intact antrum, excitatory vagal nerve stimulation increased the frequency of slow waves. Simultaneous intracellular recordings of pacemaker potentials from myenteric interstitial cells (ICC MY ) and slow waves showed that the onset of each pacemaker potential normally preceded the onset of each slow wave but vagal stimulation caused the onset of each slow wave to precede each pacemaker potential. Together the observations suggest that during vagal stimulation there is a change in the origin of pacemaker activity with slow waves being initiated by intramuscular interstitial cells (ICC IM ) rather than by ICC MY .

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