Misgeld U, Calabresi P, Dodt H U
Pflugers Arch. 1986 Nov;407(5):482-7. doi: 10.1007/BF00657504.
Intracellular recording from neostriatal neurons in rat brain slices revealed effects of the acetylcholine (ACh) agonist carbachol (Cch, 1-10 mumol/l), of the anticholinesterase physostigmine (10 mumol/l) and of the muscarinic antagonist atropine (10 mumol/l) on plateau potentials elicited in the presence of K-blockers. Plateau potentials elicited in the presence of K-blockers were Ca-dependent, since they persisted in Na-free solution, were resistant to tetrodotoxin (TTX, 3 mumol/l) and blocked by Cd (0.1-0.5 mmol/l). Cch reduced the duration of the plateau potentials and made them more susceptible to fatigue. These effects were antagonized by atropine (1-10 mumol/l), but not by Ba (100-200 mumol/l) or 4-aminopyridine (4-AP, 0.5 mmol/l). Physostigmine (10 mumol/l) had the same atropine-sensitive effects as Cch on the plateau potential. Atropine (10 mumol/l), by itself, prolonged the duration of the plateau potential. High concentrations (100 mumol/l) of Cch did not further reduce the duration of the plateau potential, instead, the duration re-increased with prolonged exposure. The re-increase of the plateau-spike duration was later masked by bursting activity. The opposing effects of low and high concentrations of Cch on the plateau potential duration corresponded to effects of this drug on intrastriatally evoked EPSPs in that low concentrations of Cch reduced the EPSP amplitude, but high concentrations re-increased it after a transient decrease. It is concluded that the muscarinic effect of ACh in the neostriatum is to modulate Ca-influx and that this effect is exerted in a tonic manner.
对大鼠脑片新纹状体神经元进行细胞内记录,结果显示乙酰胆碱(ACh)激动剂卡巴胆碱(Cch,1 - 10 μmol/L)、抗胆碱酯酶毒扁豆碱(10 μmol/L)以及毒蕈碱拮抗剂阿托品(10 μmol/L)对在钾通道阻滞剂存在时诱发的平台电位的影响。在钾通道阻滞剂存在时诱发的平台电位是钙依赖性的,因为它们在无钠溶液中持续存在,对河豚毒素(TTX,3 μmol/L)有抗性且被镉(0.1 - 0.5 mmol/L)阻断。Cch缩短了平台电位的持续时间并使其更容易疲劳。这些效应被阿托品(1 - 10 μmol/L)拮抗,但不被钡(100 - 200 μmol/L)或4 - 氨基吡啶(4 - AP,0.5 mmol/L)拮抗。毒扁豆碱(10 μmol/L)对平台电位具有与Cch相同的阿托品敏感效应。阿托品(10 μmol/L)自身可延长平台电位的持续时间。高浓度(100 μmol/L)的Cch并未进一步缩短平台电位的持续时间,相反,随着暴露时间延长,持续时间再次增加。平台峰持续时间的再次增加随后被爆发活动掩盖。低浓度和高浓度Cch对平台电位持续时间的相反作用与该药物对纹状体内诱发的兴奋性突触后电位(EPSP)的作用相对应,即低浓度的Cch降低EPSP幅度,但高浓度在短暂降低后使其再次增加。结论是,ACh在新纹状体中的毒蕈碱样作用是调节钙内流,且这种作用是以紧张性方式发挥的。