The involvement of D1 and D2 dopamine receptors in amphetamine-induced changes in striatal unit activity in behaving rats

IF 3.2 4区 医学 Q3 NEUROSCIENCES Brain Research Pub Date : 1993-08-13 Epub Date: 2003-03-06 DOI:10.1016/0006-8993(93)91633-4
Ariane Rosa-Kenig , Jerome K. Puotz , George V. Rebec
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引用次数: 34

Abstract

Selective D1 (SCH-23390) and D2 (eticlopride and sulpiride) dopamine receptor antagonists were assessed for their ability to reverse the effects of 1.0 mg/kgd-amphetamine on excitatory motor-related neurons in the striatum of freely moving rats. SCH-23390 (0.125, 0.25, 0.5 and 1.0 mg/kg) rapidly and consistently blocked amphetamine-induced neuronal excitations as did eticlopride (0.25 and 1.0 mg/kg). In contrast, (−)-sulpiride (10, 20 and 40 mg/kg) failed to alter the neuronal response to amphetamine. Similarly, SCH-23390 and eticlopride also blocked the behavioral effects of amphetamine, but sulpiride did not. Collectively, these results support the involvement of D1 and D2 dopamine receptors in the excitatory effects of amphetamine on striatal neurons, but suggest caution in assessing the neuronal and behavioral effects of sulpiride.

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多巴胺D1和D2受体参与安非他明诱导行为大鼠纹状体单位活动的改变
研究了选择性D1 (SCH-23390)和D2(依替氯pride和舒匹利)多巴胺受体拮抗剂对1.0 mg/kgd-安非他明对自由运动大鼠纹状体兴奋性运动相关神经元的逆转作用。SCH-23390(0.125、0.25、0.5和1.0 mg/kg)与依替氯pride(0.25和1.0 mg/kg)一样,能快速且持续地阻断安非他明诱导的神经元兴奋。相反,(−)-舒必利(10、20和40 mg/kg)未能改变神经元对安非他明的反应。同样,SCH-23390和依替氯pride也阻断了安非他明的行为效应,但舒必利没有。总的来说,这些结果支持D1和D2多巴胺受体参与安非他明对纹状体神经元的兴奋作用,但建议在评估舒必利对神经元和行为的影响时要谨慎。
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来源期刊
Brain Research
Brain Research 医学-神经科学
CiteScore
5.90
自引率
3.40%
发文量
268
审稿时长
47 days
期刊介绍: An international multidisciplinary journal devoted to fundamental research in the brain sciences. Brain Research publishes papers reporting interdisciplinary investigations of nervous system structure and function that are of general interest to the international community of neuroscientists. As is evident from the journals name, its scope is broad, ranging from cellular and molecular studies through systems neuroscience, cognition and disease. Invited reviews are also published; suggestions for and inquiries about potential reviews are welcomed. With the appearance of the final issue of the 2011 subscription, Vol. 67/1-2 (24 June 2011), Brain Research Reviews has ceased publication as a distinct journal separate from Brain Research. Review articles accepted for Brain Research are now published in that journal.
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