Suzuki T, Volle R L
Naunyn Schmiedebergs Arch Pharmacol. 1978 Aug;304(1):15-20. doi: 10.1007/BF00501372.
The effects of isoprenaline were studied in isolated rat superior cervical ganglia. Intracellularly recorded excitatory postsynaptic potentials were depressed by isoprenaline in concentrations of 10(-5) to 10(-4)M. In 13 out of 17 cells, isoprenaline caused ganglionic hyperpolarization (mean, 4mV). Changes in the amplitude and contour of antidromic action potentials caused by isoprenaline could be accounted for by the increased membrane potential. A slight increase in membrane input resistance from 44--50.2 megohms (mean values) occurred in about half of the cells. Activation of an ion pump by isoprenaline was suggested by the finding that the hyperpolarization did not occur when the bathing solution contained ouabain (10(-5)M) or lacked Na+ or K+. Characterization of the isoprenaline effects by the use of alpha and beta adrenergic blocking drugs was not possible because of the direct depressant effects of the antagonists. The muscarinic agonist bethanechol (2.5 X 10(-5) to 2.5 X 10(-4)M) caused ganglionic depolarization and increased input membrane resistance (42--52 megohms) during depolarization in each of the cells tested. The ganglionic responses to bethanechol were prevented by atropine.
研究了异丙肾上腺素对离体大鼠颈上神经节的作用。细胞内记录的兴奋性突触后电位在浓度为10⁻⁵至10⁻⁴M的异丙肾上腺素作用下受到抑制。在17个细胞中的13个细胞中，异丙肾上腺素引起神经节超极化（平均为4mV）。异丙肾上腺素引起的逆向动作电位幅度和波形的变化可由膜电位升高来解释。约一半的细胞中，膜输入电阻从44 - 50.2兆欧（平均值）略有增加。当浴液中含有哇巴因（10⁻⁵M）或缺乏Na⁺或K⁺时超极化未发生，这一发现提示异丙肾上腺素激活了离子泵。由于拮抗剂具有直接抑制作用，因此无法用α和β肾上腺素能阻断药物来表征异丙肾上腺素的作用。毒蕈碱激动剂氨甲酰甲胆碱（2.5×10⁻⁵至2.5×10⁻⁴M）在每个测试细胞中引起神经节去极化，并在去极化期间增加输入膜电阻（42 - 52兆欧）。阿托品可阻断神经节对氨甲酰甲胆碱的反应。
