Popoli P, Caporali M G, Scotti de Carolis A
Laboratorio di Farmacologia, Istituto Superiore di Sanità, Rome, Italy.
Pharmacol Biochem Behav. 1989 Jan;32(1):203-6. doi: 10.1016/0091-3057(89)90234-7.
A behavioral study on the stereotypy induced by caffeine and carbamazepine or caffeine and haloperidol was assessed in adult male rabbits. The stereotypy induced by caffeine + carbamazepine was not reduced by pretreatment with haloperidol (0.1 mg/kg) or SCH 23390 (0.01 mg/kg). N-ethylcarboxamidoadenosine (NECA, 0.01 mg/kg), an A2 adenosine receptor agonist, completely prevented the appearance of caffeine + carbamazepine-, but not of caffeine + haloperidol-induced stereotypy. An EEG investigation was also performed in order to evaluate the influence of the blockade of D-1 and D-2 dopamine receptors on the desynchronized tracing induced by caffeine (50 mg/kg). Neither haloperidol (0.1 mg/kg) nor SCH 23390 (0.01 mg/kg) were able to influence this EEG effect of caffeine. Present data support the hypothesis that A2 adenosine receptors may be involved in the control of pathological movements. The relationship between the purinergic system and D-1/D-2 dopamine receptors is also discussed.
在成年雄性兔子中评估了咖啡因与卡马西平或咖啡因与氟哌啶醇诱导的刻板行为的一项行为学研究。氟哌啶醇（0.1毫克/千克）或SCH 23390（0.01毫克/千克）预处理并未减轻咖啡因+卡马西平诱导的刻板行为。A2腺苷受体激动剂N - 乙基羧酰胺腺苷（NECA，0.01毫克/千克）完全阻止了咖啡因+卡马西平诱导的刻板行为的出现，但未阻止咖啡因+氟哌啶醇诱导的刻板行为。还进行了脑电图研究，以评估D - 1和D - 2多巴胺受体阻断对咖啡因（50毫克/千克）诱导的去同步化脑电图描记的影响。氟哌啶醇（0.1毫克/千克）和SCH 23390（0.01毫克/千克）均无法影响咖啡因的这种脑电图效应。现有数据支持A2腺苷受体可能参与病理性运动控制的假说。还讨论了嘌呤能系统与D - 1/D - 2多巴胺受体之间的关系。
