Przegaliński E, Filip M
Institute of Pharmacology, Polish Academy of Sciences, Kraków, Poland.
Pol J Pharmacol. 1997 Sep-Oct;49(5):291-8.
The effects of the NO donor molsidomine and the inhibitors of the NO synthase (NOS) 7-nitroindazole (7-NI) and NG-nitro-L-arginine methyl ester (L-NAME) on the motor hyperactivity induced by indirect (amphetamine and cocaine) or direct (SKF 38393 and bromocriptine) dopamine (DA) agonists were studied in rats. The hyperactivity induced by 0.5 mg/kg of amphetamine or 5 mg/kg of cocaine was potentiated in a dose-dependent manner by molsidomine (30-100 mg/kg), but attenuated by 7-NI (3-30 mg/kg) or L-NAME (3-30 mg/kg). The NOS inhibitors also inhibited the locomotor hyperactivity evoked by 15 mg/kg of SKF 38393 (a DA D1 agonist) or 5 mg/kg of bromocriptine (a DA D2 agonist). On the other hand, the hyperactivity induced by those direct DA receptor agonists was potentiated by molsidomine. The present findings provide further evidence for an interaction at the behavioral level between NO and the DA-mediated effects of amphetamine and cocaine; moreover, they seem to indicate that both DA D1 and DA D2 receptor subtypes are under such influence.
在大鼠中研究了一氧化氮（NO）供体吗多明以及NO合酶（NOS）抑制剂7-硝基吲唑（7-NI）和N-硝基-L-精氨酸甲酯（L-NAME）对间接（苯丙胺和可卡因）或直接（SKF 38393和溴隐亭）多巴胺（DA）激动剂诱导的运动亢进的影响。吗多明（30 - 100mg/kg）以剂量依赖的方式增强了0.5mg/kg苯丙胺或5mg/kg可卡因诱导的运动亢进，但7-NI（3 - 30mg/kg）或L-NAME（3 - 30mg/kg）则减弱了这种运动亢进。NOS抑制剂还抑制了15mg/kg SKF 38393（一种DA D1激动剂）或5mg/kg溴隐亭（一种DA D2激动剂）引起的运动亢进。另一方面，吗多明增强了那些直接DA受体激动剂诱导的运动亢进。本研究结果为NO与苯丙胺和可卡因的DA介导效应在行为水平上的相互作用提供了进一步的证据；此外，它们似乎表明DA D1和DA D2受体亚型均受这种影响。
