The potential involvement of the muscarinic cholinergic system in the underlying mechanisms of prepulse inhibition of the acoustic startle reflex was evaluated in male Sprague-Dawley rats under conditions of varying dose, prepulse intensity, and interstimulus interval. The effects of scopolamine on prepulse inhibition were also directly compared with the effects observed using apomorphine and phencyclidine under the same test parameters. Scopolamine (0. 03-1.0 mg/kg) produced a significant dose-dependent decrease in prepulse inhibition, but had no effect on startle amplitude over the dose range tested. Apomorphine (0.03-1.0 mg/kg) and phencyclidine (0. 1-5.6 mg/kg) produced significant dose-dependent decreases in prepulse inhibition and changes in startle amplitude. The scopolamine-induced decrease in prepulse inhibition varied with prepulse intensity in that the changes produced by scopolamine became smaller in magnitude as the prepulse intensity was increased from 9 to 30 dB above background. On the other hand, apomorphine and phencyclidine decreased prepulse inhibition to approximately the same magnitude across all prepulse intensities tested. The observed decreases in prepulse inhibition produced by scopolamine, apomorphine, and phencyclidine were also dependent on interstimulus interval duration. Scopolamine produced marked decreases in prepulse inhibition at the 100- and 300-ms interstimulus interval durations, but had little or no effect on prepulse inhibition at the 30- and 1000-ms interstimulus interval durations. In contrast, apomorphine decreased prepulse inhibition across all interstimulus interval durations while phencyclidine decreased prepulse inhibition across the 30- to 300-ms interstimulus interval durations. The present findings support the hypothesis that the muscarinic cholinergic system, like the dopaminergic and glutamatergic systems, is directly involved in the mechanisms of prepulse inhibition. However, these three neurotransmitter systems appear to modulate different aspects of prepulse inhibition.

译文

:在不同剂量,前脉冲强度和刺激间隔的条件下,对雄性Sprague-Dawley大鼠评估了毒蕈碱胆碱能系统潜在地参与声惊跳反射的预脉冲抑制的潜在机制。还可以将东parameters碱对脉冲前抑制的作用与在相同测试参数下使用阿扑吗啡和苯环利定所观察到的作用直接进行比较。东co碱(0. 03-1.0 mg / kg)在前脉冲抑制中产生明显的剂量依赖性降低,但在所测试的剂量范围内对惊吓幅度没有影响。阿扑吗啡(0.03-1.0 mg / kg)和苯环利定(0. 1-5.6 mg / kg)在前脉冲抑制和惊吓振幅变化中产生显着的剂量依赖性降低。东碱引起的前脉冲抑制的降低随前脉冲强度的变化而变化,因为东as碱所产生的变化幅度随前脉冲强度从背景值的9 dB增加到30 dB而变小。另一方面,在所有测试的前脉冲强度中,阿扑吗啡和苯环利定将前脉冲抑制作用降低至大致相同的大小。观察到的东po碱,阿扑吗啡和苯环利定产生的前冲抑制作用的减少还取决于刺激间隔时间。东co碱在100和300毫秒的刺激间隔时间产生的前脉冲抑制作用显着降低,但在30和1000毫秒的刺激间隔时间对前脉冲抑制作用很小或没有影响。相反,阿扑吗啡在所有刺激间隔期间降低了脉冲前抑制,而苯环利定在30-300ms刺激间隔期间降低了前脉冲抑制。本发现支持以下假设:毒蕈碱胆碱能系统,如多巴胺能和谷氨酸能系统,直接参与前脉冲抑制的机制。但是,这三个神经递质系统似乎调节前脉冲抑制的不同方面。

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