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Atropine‐resistant depolarization in the guinea‐pig small intestine
Author(s) -
Bywater R. A. R.,
Holman M. E.,
Taylor G. S.
Publication year - 1981
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.1981.sp013794
Subject(s) - hyperpolarization (physics) , depolarization , apamin , membrane potential , excitatory postsynaptic potential , biophysics , stimulation , chemistry , inhibitory postsynaptic potential , tetrodotoxin , atropine , resting potential , potassium channel , endocrinology , biology , stereochemistry , nuclear magnetic resonance spectroscopy
1. Junction potentials were recorded from the circular muscle cells of the guinea‐pig ileum following transmural stimulation in the presence of atropine at 30 °C. 2. Single stimuli produced a transient hyperpolarization, the inhibitory junction potential (i.j.p.). At high stimulus strengths the i.j.p. was followed by a post‐stimulus depolarization (PSD). 3. During repetitive stimulation the magnitude of the hyperpolarization decreased; however, at the end of the stimulus period the PSD was enhanced and often reached threshold for the generation of action potentials. Thus, the size of the PSD was not directly related to the degree of the preceding hyperpolarization. 4. Hyperpolarization of the circular muscle cells was produced by the application of anodal current using large external electrodes. Rapid cessation of the applied current produced a transient after‐depolarization which was shorter in time course than the PSD following the i.j.p. If the applied anodal current was reduced slowly (at a rate which mimicked the decrease in the hyperpolarization during repetitive nerve stimulation) no after‐depolarization was observed. 5. Conditioning hyperpolarization of the circular muscle cells reduced the amplitude of the i.j.p. The i.j.p. was reversed at membrane potentials greater than approximately ‐90 mV. 6. The PSD did not appear to be due to the extracellular accumulation of potassium ions following the i.j.p. since the PSD persisted even when the i.j.p. was reversed. 7. The neurotoxin apamin reversibly abolished the i.j.p. and unmasked a transient excitatory junction potential (e.j.p.) with a variable latency (350‐900 ms).