Daniel E E, Helmy-Elkholy A, Jager L P, Kannan M S
J Physiol. 1983 Mar;336:243-60. doi: 10.1113/jphysiol.1983.sp014579.
Effects of stimulation of intramural nerves in the circular smooth muscle layer of the body of the oesophagus of the opossum (Didelphis marsupialis) were studied, simultaneously measuring the membrane potential of muscle cells using the sucrose-gap technique and contractions of the muscle. Electrical field stimulation of the preparation, superfused with Krebs solution at 27 degrees C, induced a transient hyperpolarization of the smooth muscle cell membrane (i.j.p.) followed by a transient depolarization on which muscle action potentials were often superimposed. The muscle did not develop active tension spontaneously; it therefore did not relax during the i.j.p., but often contracted during the 'off' depolarization. The i.j.p. and the responses following it were characterized as mediated by intramural, non-adrenergic, non-cholinergic (n.a.n.c.) nerves. The i.j.p. amplitude was reduced by raising the external K concentration. When Cl was replaced by isethionate, a small hyperpolarization of the smooth muscle cell membrane ensued along with a comparable small reduction of the i.j.p. amplitude. The 'off' activity following the i.j.p. disappeared completely in Cl-free medium. Apamin (10(-7)-10(-5) M) did not influence this preparation nor the i.j.p. Adenosine and its related adenine nucleotides in concentrations up to 10(-3) M hardly affected the preparation. Prolonged superfusion with adenosine and 6-chloroadenosine revealed a gradually increasing attenuation of the i.j.p. Exogenously applied vasoactive intestinal polypeptide (VIP) induced rhythmic depolarizations of the smooth muscle cell membrane and spontaneous contractions, which were insensitive to neurotoxins but absent in Cl-free media. Field stimulation in the presence of VIP caused an i.j.p. which transiently interrupted the VIP-induced contractile responses. It is concluded that the inhibitory mediator of the intramural n.a.n.c. nerves present in the circular smooth muscle layer of the opossum oesophagus is neither a purine nor VIP. The i.j.p. may result from a selective increase in K permeability of the smooth muscle cell membrane, the 'off' depolarization may involve an increase in the Cl ion conductance. The suggestion is made that the release of neurotransmitter from intramural n.a.n.c. nerves is modulated presynaptically via P1-purinoceptors and that VIP is a likely candidate for an excitatory transmitter, released simultaneously with the inhibitory transmitter.
研究了对负鼠（Didelphis marsupialis）食管体环形平滑肌层壁内神经的刺激效应，同时使用蔗糖间隙技术测量肌肉细胞的膜电位和肌肉收缩情况。在27摄氏度下用 Krebs 溶液灌流标本，进行电场刺激，可诱导平滑肌细胞膜短暂超极化（抑制性接头电位），随后是短暂去极化，肌肉动作电位常叠加在该去极化之上。肌肉不会自发产生主动张力；因此在抑制性接头电位期间不会松弛，但在“去极化”期常收缩。抑制性接头电位及其后续反应的特征是由壁内非肾上腺素能、非胆碱能（n.a.n.c.）神经介导。提高细胞外钾浓度会降低抑制性接头电位的幅度。当用羟乙基磺酸替代氯离子时，平滑肌细胞膜会出现轻微超极化，同时抑制性接头电位幅度也有类似程度的减小。在无氯培养基中，抑制性接头电位后的“去极化”活动完全消失。蜂毒明肽（10⁻⁷ - 10⁻⁵ M）对该标本和抑制性接头电位均无影响。浓度高达10⁻³ M 的腺苷及其相关腺嘌呤核苷酸对标本影响很小。用腺苷和6 - 氯腺苷长时间灌流显示抑制性接头电位逐渐衰减。外源性应用血管活性肠肽（VIP）可诱导平滑肌细胞膜节律性去极化和自发收缩，这些反应对神经毒素不敏感，但在无氯培养基中不存在。在VIP存在的情况下进行电场刺激会产生抑制性接头电位，该电位会短暂中断VIP诱导的收缩反应。得出的结论是，负鼠食管环形平滑肌层中存在的壁内n.a.n.c.神经的抑制性介质既不是嘌呤也不是VIP。抑制性接头电位可能是平滑肌细胞膜钾通透性选择性增加的结果，“去极化”可能涉及氯离子电导增加。有人提出壁内n.a.n.c.神经递质的释放通过P1 - 嘌呤受体在突触前受到调节，并且VIP可能是一种兴奋性递质的候选物，与抑制性递质同时释放。
