Akasu T, Gallagher J P, Nakamura T, Shinnick-Gallagher P, Yoshimura M
J Physiol. 1985 Apr;361:165-84. doi: 10.1113/jphysiol.1985.sp015639.
Responses to noradrenaline (NA) applied by superfusion, ionophoresis or pressure pulse were analysed using conventional intracellular recording and voltage-clamp methods in cat vesical parasympathetic ganglia. NA (1 microM) hyperpolarized 60% of the neurones, depolarized 25%, and produced a biphasic potential, which comprised a membrane hyperpolarization followed by a membrane depolarization, in 10%. About 5% of the neurones did not respond to NA. The NA hyperpolarization was blocked by yohimbine (1 microM), an alpha 2-adrenoceptor antagonist, whereas the NA depolarization was blocked by prazosin (0.1-1 microM), an alpha 1-adrenoceptor antagonist. These data indicated that the NA hyperpolarization was mediated through alpha 2-adrenoceptors and the NA depolarization through alpha 1-adrenoceptors. The NA hyperpolarization was accompanied by an increase in conductance, while the NA depolarization was associated with a decrease in conductance measured under manual-clamp conditions. Similar conductance changes were observed under voltage clamp. NA hyperpolarizations became smaller as the membrane was hyperpolarized and reversed polarity beyond -100 mV. NA depolarizations also became smaller at hyperpolarized membrane potentials and reversed polarity around -90 mV. The NA responses were enhanced in low-K media and depressed in high-K Krebs solution. The NA hyperpolarization was blocked by the Ca antagonists, Cd, Mn and Co. Intracellular injection of EGTA caused a slowly developing, progressive block of the NA hyperpolarization. The NA depolarization was not affected by low Ca concentrations, Ca antagonists or intracellular injection of EGTA. In some neurones the NA depolarization was unmasked in solutions containing Ca antagonists and after intracellular EGTA injection. The NA hyperpolarization was depressed by intracellular injection and extracellular superfusion of Cs but not by TEA. Ba (10-100 microM) depressed the NA hyperpolarization by 30%. The NA depolarization persisted in the presence of muscarine (10 microM) and was not blocked by Cs or TEA but was depressed 70% by Ba (10 microM). These data are consistent with the hypotheses that alpha 2-adrenoceptor activation produces a membrane hyperpolarization that is mediated through a Ca-dependent K conductance, and that alpha 1-adrenoceptor activation produces a membrane depolarization through closure of a voltage-insensitive K channel.
在猫膀胱副交感神经节中，使用传统的细胞内记录和电压钳方法，分析了通过灌流、离子电泳或压力脉冲施加去甲肾上腺素（NA）后的反应。NA（1微摩尔）使60%的神经元超极化，25%的神经元去极化，10%的神经元产生双相电位，即先出现膜超极化，随后是膜去极化。约5%的神经元对NA无反应。NA超极化被α2肾上腺素能受体拮抗剂育亨宾（1微摩尔）阻断，而NA去极化被α1肾上腺素能受体拮抗剂哌唑嗪（0.1 - 1微摩尔）阻断。这些数据表明，NA超极化是通过α2肾上腺素能受体介导的，而NA去极化是通过α1肾上腺素能受体介导的。NA超极化伴随着电导增加，而在手动钳制条件下测量时，NA去极化与电导降低有关。在电压钳下也观察到类似的电导变化。随着膜超极化，NA超极化变小，在超过 -100 mV时极性反转。在超极化的膜电位下，NA去极化也变小，并在 -90 mV左右极性反转。在低钾培养基中NA反应增强，而在高钾Krebs溶液中受到抑制。NA超极化被钙拮抗剂Cd、Mn和Co阻断。细胞内注射EGTA导致NA超极化缓慢发展并逐渐被阻断。NA去极化不受低钙浓度、钙拮抗剂或细胞内注射EGTA的影响。在一些神经元中，在含有钙拮抗剂的溶液中以及细胞内注射EGTA后，NA去极化被暴露出来。细胞内注射和细胞外灌流Cs可抑制NA超极化，但TEA无此作用。Ba（10 - 100微摩尔）使NA超极化降低30%。在毒蕈碱（10微摩尔）存在的情况下，NA去极化持续存在，且不被Cs或TEA阻断，但被Ba（10微摩尔）降低70%。这些数据与以下假设一致：α2肾上腺素能受体激活产生通过钙依赖性钾电导介导的膜超极化，而α1肾上腺素能受体激活通过关闭电压不敏感钾通道产生膜去极化。
