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Nicotinic and muscarinic ACh receptors in rhythmically active spinal neurones in the Xenopus laevis embryo.
Author(s) -
Perrins R,
Roberts A
Publication year - 1994
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.1994.sp020244
Subject(s) - nicotinic antagonist , nicotinic agonist , mecamylamine , muscarinic acetylcholine receptor , muscarine , acetylcholine , hexamethonium , chemistry , oxotremorine , methyllycaconitine , strychnine , endocrinology , reversal potential , depolarization , medicine , neuroscience , nicotinic acetylcholine receptor , biology , receptor , biochemistry , patch clamp
1. Intracellular recordings were made from presumed motoneurones in the Xenopus embryo spinal cord, and their response to cholinergic agents was investigated. Nicotine and 1,1‐dimethyl‐4‐phenylpiperazinium (DMPP; both 1‐10 microM) strongly depolarized, and muscarine and oxotremorine (2‐20 microM) weakly hyperpolarized, these neurones. Tetrodotoxin (1 microM), which blocks action potentials in Xenopus neurones, did not affect either of these responses. 2. The extrapolated reversal potential of the nicotinic depolarization was ‐12.1 +/‐ 8.3 mV (mean +/‐ S.E.M.) suggesting the opening of a mixed conductance. The nicotinic response was antagonized by dihydro‐beta‐erythroidine, d‐tubocurarine and mecamylamine (10‐20 microM) but not by alpha‐bungarotoxin (10 microM). 3. The muscarinic response was not reversed when recorded with electrodes filled with potassium chloride but was antagonized by atropine (0.1 microM). 4. Acetylcholine (ACh, 10 microM) caused a strong depolarization of the neurones which was blocked by d‐tubocurarine and dihydro‐beta‐erythroidine, suggesting that its effects are mediated predominantly by nicotinic ACh receptors. 5. ACh and nicotinic agonists applied to the spinal cord produced a barrage of IPSPs that were blocked by TTX and strychnine.