Ambache N, Killick S W, Zar M A
Br J Pharmacol. 1974 Oct;52(2):175-90. doi: 10.1111/j.1476-5381.1974.tb09698.x.
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-dimethylammonium-phenyl)-pentan-3-one dibromide) and iso-OMPA (tetramonoisopropylpyrophosphortetramide), 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 muM) even after cholinesterase inhibition, suggesting an absence of ganglion-cells; with nicotine (105-210 muM) 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 alpha-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.
兔直肠尾骨肌的孤立、去鞘制剂对除毒蕈碱类药物以外的致痉剂相对不敏感。用1 - 50个脉冲（10Hz时0.2 - 0.4ms）进行透壁刺激可引起分级的抽搐，这些抽搐被河豚毒素消除，因此是神经源性的；较长的脉冲有时会引发对河豚毒素耐药的肌源性收缩。
0.2 - 0.4ms脉冲引起的抽搐是由于节后兴奋，因为六甲铵、潘托铵或二甲基筒箭毒碱，或尼古丁的神经节麻痹浓度均不能使其减弱。
用测压法测定了直肠尾骨肌的乙酰胆碱酯酶和丁酰胆碱酯酶活性，BW 284C51（1:5 - 双 -（4 - 烯丙基 - 二甲基铵 - 苯基） - 戊烷 - 3 - 酮二溴化物）和异 - OMPA（四单异丙基焦磷酰胺）可分别选择性抑制它们。只有当两种胆碱酯酶都被抑制时，单脉冲抽搐的幅度和持续时间才会大大增强。
即使在胆碱酯酶抑制后，尼古丁（2.1 - 21μM）也不能使制剂收缩，这表明不存在神经节细胞；使用尼古丁（105 - 210μM）时，会引发小的、对阿托品敏感的反应，这些反应是非神经节性的，因为它们不会被河豚毒素减弱。
用毒扁豆碱处理过的直肠尾骨肌制剂在电刺激时会将乙酰胆碱释放到浴液中。
运动传递被肉毒杆菌毒素（A型）麻痹，被阿托品消除；阿托品对毒蕈碱受体的阻断对内源性和外源性乙酰胆碱均有效。
在平滑肌中检测到抑制性肾上腺素能受体和少量运动性α - 肾上腺素能受体。
去甲肾上腺素（但酪胺不行）、异丙肾上腺素，以及在酚妥拉明之后的肾上腺素和去氧肾上腺素，均能强烈抑制运动传递和节律性活动。普萘洛尔只能轻微减弱这些抑制作用，而吲哚洛尔的作用更强。
对保留其外在神经供应的制剂进行的实验表明，在该肌肉运动神经通路的最后1 - 2cm处不存在神经节中继。
描述了相邻的尾 - 肛门肌的一些对比特性，包括对透壁刺激的运动反应较差。
