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Ongoing Nicotinic And Non‐Nicotinic Inputs To Inhibitory Neurons In The Mouse Colon
Author(s) -
Powell Andrew K,
Fida Rosa,
Bywater Robert AR
Publication year - 2001
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1046/j.1440-1681.2001.03524.x
Subject(s) - hexamethonium , apamin , inhibitory postsynaptic potential , chemistry , nicotinic agonist , endocrinology , medicine , biophysics , pharmacology , potassium channel , receptor , biology , biochemistry
SUMMARY 1. Intracellular microelectrodes were used to record spontaneous and evoked inhibitory junction potentials (IJP) from the circular muscle layer of the mid‐distal region of the mouse isolated colon in the presence of nifedipine (1 μmol/L) and hyoscine (1 μmol/L). 2. The length of the tissue preparation (> 1 cm) or the presence of the mucosa had no effect on the frequency of spontaneous IJP. 3. Hexamethonium (500 μmol/L) reduced the frequency of spontaneous IJP to approximately 70% of the control frequency, whereas D ‐tubocurarine (280 μmol/L) reduced the frequency to approximately 17% of control. Apamin (250 nmol/L) abolished all spontaneous IJP activity. 4. The greater inhibition of spontaneous IJP in the presence of D ‐tubocurarine compared with hexamethonium is discussed as a possible ‘apamin‐like’ effect. 5. Although electrically evoked IJP (single pulse at 15 V, 0.6 msec) were not significantly affected by hexamethonium, D ‐tubocurarine and apamin reduced the amplitude of evoked IJP to approximately 65 and 50% of control, respectively. 6. These results suggest that the properties of spontaneous IJP cannot be inferred by a study of evoked IJP alone.