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THE RABBIT RECTOCOCCYGEUS: A GANGLION‐FREE, PARASYMPATHETICALLY INNERVATED PREPARATION
Author(s) -
AMBACHE N.,
KILLICK S.W.,
ZAR M. ABOO
Publication year - 1974
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1974.tb09698.x
Subject(s) - hexamethonium , atropine , physostigmine , muscarinic acetylcholine receptor , tetrodotoxin , acetylcholine , chemistry , neuromuscular transmission , stimulation , cholinesterase , endocrinology , medicine , inhibitory postsynaptic potential , pharmacology , receptor , biochemistry , biology
1 Isolated, desheathed preparations of the rabbit rectococcygeus muscle were relatively insensitive to spasmogens other than muscarinic drugs. Transmural stimulation with 1–50 pulses (0.2–0.4 ms at 10 Hz) elicited graded twitches which were abolished by tetrodotoxin and were therefore neurogenic; longer pulses sometimes triggered tetrodotoxin‐resistant myogenic contractions. 2 Twitches elicited by 0.2–0.4 ms pulses were due to post‐ganglionic excitation because they were not reduced by hexamethonium, pentolinium or dimethyltubocurarine, or by ganglion‐paralyzing concentrations of nicotine. 3 The acetyl‐ and butyryl‐cholinesterase activities of the rectococcygeus were determined manometrically and could be selectively inhibited by BW 284C51 (1:5‐bis‐(4‐allyl‐dimethyl‐ammonium‐phenyl)‐pentan‐3‐one dibromide) and iso ‐OMPA (tetramono iso propylpyrophosphortetramide), respectively. Single‐pulse twitches were greatly potentiated in amplitude and duration only when both cholinesterases were inhibited. 4 The preparations could not be made to contract by nicotine (2.1–21 μ m ) even after cholinesterase inhibition, suggesting an absence of ganglion‐cells; with nicotine (105–210 μ m ) small, atropine‐susceptible responses were elicited, which were non‐ganglionic because they were not reduced by tetrodotoxin. 5 Rectococcygeus preparations that had been treated with physostigmine released acetylcholine into the bath fluid on electrical stimulation. 6 The motor transmission was paralyzed by botulinum toxin (Type A) and abolished by atropine; the block of muscarinic receptors by atropine was effective against both endogenous and exogenous acetylcholine. 7 Inhibitory adrenoceptors and scanty motor α‐adrenoceptors were detected in the smooth muscle. 8 Strong inhibitions of motor transmission and of rhythmic activity were produced by noradrenaline (but not by tyramine), by isoprenaline, and, after phentolamine, also by adrenaline and phenylephrine. These inhibitions were only slightly reduced by propranolol and rather more by pindolol. 9 Experiments on preparations retaining their extrinsic nerve supply suggest an absence of ganglionic relays in the last 1–2 cm of the motor nerve pathway to this muscle. 10 Some contrasting properties of the adjacent caudo‐anal muscle, including the poor motor responses to transmural stimulation, are described.