Laboratory of Physiology, Department of Basic Veterinary Science, The United Graduate School of Veterinary Sciences, Gifu University, Japan.
Auton Neurosci. 2012 May 21;168(1-2):25-31. doi: 10.1016/j.autneu.2012.01.003. Epub 2012 Jan 30.
In the present study, we characterized the neural regulation of esophageal striated muscle in Suncus murinus (a house musk shrew; "suncus" used as a laboratory name), which was compared with that in the rat. The tunica muscularis consists of striated muscle in the suncus esophagus. An isolated segment of the suncus esophagus was placed in an organ bath and the contractile responses were recorded using a force transducer. Electrical stimulations to vagus nerves induced contractile responses in the esophageal segment. Treatment with α-bungarotoxin, a blocker of nicotinic acetylcholine receptors, blocked the vagally mediated contractions of the suncus esophagus. D-tubocurarine and succinylcholine, typical antagonists of nicotinic acetylcholine receptors, also inhibited the suncus esophageal contractions, while higher concentrations of the agents were required rather than concentrations for producing an equivalent block in the rat. We used capsaicin, a stimulator of small-caliber afferent neurons, for activating the peripheral neural network. The reagent inhibited the vagally mediated twitch contractions of striated muscle in the suncus esophagus, which was reversed by pretreatment with a nitric oxide synthase inhibitor, N(G)-nitro-L-arginine methyl ester. Application of a nitric oxide donor, diethylamine NONOate diethylammonium salt, mimicked capsaicin-induced inhibition. The results suggest that motility of the suncus esophagus, which consists of striated muscles, is regulated by vagal cholinergic neurons. The local neural network including capsaicin-sensitive neurons and intrinsic nitrergic neurons can modify the vagally mediated motility in the suncus esophagus. In addition, nicotinic acetylcholine receptors of the suncus esophagus might be pharmacologically distinct from those of rodent esophagi.
在本研究中,我们对食蟹猴(一种家鼠狐猴;“suncus”用作实验室名称)的食管横纹肌的神经调节进行了描述,并与大鼠进行了比较。食蟹猴的食管壁由横纹肌组成。将食蟹猴食管的一段分离出来,放入器官浴槽中,使用力传感器记录收缩反应。电刺激迷走神经可引起食管段的收缩反应。用α-银环蛇毒素(烟碱型乙酰胆碱受体的阻断剂)处理可阻断迷走神经介导的食蟹猴食管收缩。D-筒箭毒碱和琥珀酰胆碱是烟碱型乙酰胆碱受体的典型拮抗剂,也抑制了食蟹猴食管的收缩,而所需的浓度高于在大鼠中产生等效阻断所需的浓度。我们使用辣椒素(一种小直径传入神经元的刺激剂)来激活周围神经网络。该试剂抑制了食蟹猴食管横纹肌的迷走神经介导的抽搐收缩,用一氧化氮合酶抑制剂 N(G)-硝基-L-精氨酸甲酯预处理可逆转这种抑制。一氧化氮供体二乙氨乙基硝胺(diethylamine NONOate diethylammonium salt)的应用模拟了辣椒素诱导的抑制作用。结果表明,由横纹肌组成的食蟹猴食管的运动受迷走胆碱能神经元调节。包括辣椒素敏感神经元和内在的氮能神经元在内的局部神经网络可以调节食蟹猴食管的迷走神经介导的运动。此外,食蟹猴食管的烟碱型乙酰胆碱受体可能在药理学上与啮齿动物食管的受体不同。