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首页> 外文期刊>The European Journal of Neuroscience >Electrophysiological evidence for a reciprocal interaction between amphetamine and cocaine-related drugs on rat midbrain dopaminergic neurons.
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Electrophysiological evidence for a reciprocal interaction between amphetamine and cocaine-related drugs on rat midbrain dopaminergic neurons.

机译：苯丙胺与可卡因相关药物在大鼠中脑多巴胺能神经元之间相互作用的电生理证据。

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摘要

To determine the functional interactions occurring between amphetamine and cocaine-like drugs on a single neuron, we used intracellular single-electrode voltage-clamp recordings from dopaminergic cells of the rat midbrain maintained in vitro. In the presence of cocaine (3-30 microM), the outward current caused by amphetamine (100 microM) on cells held at about -60 mV was attenuated. The degree of attenuation of the amphetamine-induced response was almost the same for 3 and 30 microM cocaine (44 and 51% of control, respectively). This effect of cocaine was reversible. We also tested other DA-uptake inhibitors (nomifensine and 4-phenyltetrahydroisoquinoline) against the amphetamine-induced outward current. Both drugs enhanced the effects of dopamine (DA) while reducing the outward response caused by amphetamine. Pretreatment of the animals with reserpine (12 mg/kg/i.p.), which irreversibly depletes the vesicular DA stores, neither affected the amplitude of the current caused by amphetamine nor changed the cocaine-induced attenuation of the membrane responses to amphetamine. Interestingly, when amphetamine (3 microM) was superfused on the dopaminergic neurons prior and during the application of cocaine, the DA-uptake blocker was no longer able to potentiate the outward response caused by the superfusion of DA. Taken together, these data suggest that: (i) amphetamine and cocaine interact with the DA transporter to produce distinct actions which under certain circumstances can compete with each other; (ii) the amphetamine-induced release of DA from the somata and dendrites of the dopaminergic cells is, at least in part, related to the reverse operation of the DA transporter and is not dependent on the integrity of the vesicular content of the catecholamine.
机译：为了确定在单个神经元上苯丙胺与可卡因样药物之间发生的功能相互作用，我们使用了体外维持的大鼠中脑多巴胺能细胞的细胞内单电极电压钳记录。在可卡因（3-30 microM）的存在下，苯丙胺（100 microM）对保持在约-60 mV的细胞造成的向外电流减弱。对于3和30 microM可卡因，苯丙胺引起的反应的减弱程度几乎相同（分别为对照组的44％和51％）。可卡因的这种作用是可逆的。我们还针对苯丙胺诱导的外向电流测试了其他DA摄取抑制剂（诺非芬辛和4-苯基四氢异喹啉）。两种药物都增强了多巴胺（DA）的作用，同时减少了由苯丙胺引起的向外反应。用利血平（12 mg / kg / i.p。）对动物进行预处理，这会不可逆地耗尽水泡DA的储存量，既不会影响苯丙胺引起的电流振幅，也不会改变可卡因引起的对苯丙胺的膜反应减弱。有趣的是，在可卡因使用之前和期间，在多巴胺能神经元上安非他命（3 microM）时，DA吸收阻滞剂不再能够增强由DA过量引起的向外反应。综合来看，这些数据表明：（i）苯丙胺和可卡因与DA转运蛋白相互作用，产生独特的作用，在某些情况下可以相互竞争; （ii）苯丙胺诱导的多巴胺能细胞的体细胞和树突中DA的释放至少部分地与DA转运蛋白的反向操作有关，并且不依赖于儿茶酚胺的囊泡内容物的完整性。

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