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Evidence That Acetylcholine Is An Inhibitory Transmitter Of Heart Interneurons In The Leech
Author(s) -
Joachim Schmidt,
Ronald L. Calabrese
Publication year - 1992
Publication title -
journal of experimental biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.367
H-Index - 185
eISSN - 1477-9145
pISSN - 0022-0949
DOI - 10.1242/jeb.171.1.329
Subject(s) - inhibitory postsynaptic potential , carbachol , postsynaptic potential , acetylcholine , bicuculline , hirudo medicinalis , microbiology and biotechnology , chemistry , neuroscience , muscarinic acetylcholine receptor , biology , biophysics , leech , endocrinology , receptor , biochemistry , gabaa receptor , stimulation , world wide web , computer science
1. In the leech, synaptic transmission between heart interneurons (HN cells) and between HN cells and heart motor neurons (HE cells) is blocked by bicuculline methiodide. 2. Gamma-aminobutyric acid, when applied focally onto the somata of HN cells or when added to the superfusate, has no effect on the membrane potential of HN cells. 3. Both acetylcholine (ACh) and the ACh agonist carbachol hyperpolarize HN cells and HE cells when applied focally onto their somata or into the neuropil or when added to the superfusate. 4. Inhibitory postsynaptic-potential-like responses elicited by focal application of carbachol onto the somata of HN cells and HE cells are blocked by bicuculline methiodide and are reversed when Cl- is injected into the cells. 5. Focal application of carbachol onto the somata of HN cells and HE cells increases membrane conductance. 6. The results indicate that HN cells use ACh as an inhibitory transmitter, that the postsynaptic receptors for ACh are blocked by bicuculline methiodide and that inhibition of HN cells and HE cells is mediated by an increased Cl- conductance.

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