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首页> 外文期刊>The Journal of Pharmacology and Experimental Therapeutics: Official Publication of the American Society for Pharmacology and Experimental Therapeutics >Electrophysiological Effects of Cocaethylene,Cocaine,and Ethanol on Dopaminergic Neurons of the Ventral Tegmental Area
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Electrophysiological Effects of Cocaethylene,Cocaine,and Ethanol on Dopaminergic Neurons of the Ventral Tegmental Area

机译：可卡乙烯，可卡因和乙醇对腹侧被盖区多巴胺能神经元的电生理作用

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摘要

Coabuse of ethanol and cocaine is one of the most commonly used drug combinations and results in the formation of coca- ethylene by the liver. Oopaminergic neurons of the ventral tegmental area (VT A) playa key role in the rewarding properties of drugs of abuse, including ethanol and cocaine. We have previously examined the electrophysiological effects of ethanol and cocaine, and their combined effects on these neurons. The present study investigates the electrophysiological effects of cocaethylene on dopaminergic VTA neurons with extracellular single-unit recording in brain slices from Fischer 344 rats. Co- caethylene (1-10 JLM) decreased the firing rate of dopaminergic VTA neurons, similar to the effect of cocaine over this concen- tration range. This inhibition was blocked by the O2 dopamine receptor antaQonist, sulpiride (2 JLM). At a lower concentration. cocaethylene (500 nM) potentiated ethanol-induced excitation of these neurons, similar to the effect of cocaine (500 nM) previously reported. This potentiation of ethanol excitation by cocaethylene was reversed by the 5-HT 2 antagonist ketanserin (5 ,LLM). These data suggest that cocaethylene acts through a serotonergic mechanism at low concentrations to potentiate ethanol excitation of reward neurons and through a dopami- nergic mechanism at high concentrations. The potency of co- caethylene in both of these actions is similar to that of cocaine. These effects of cocaethylene are likely to contribute to the synergistic effect on the dopaminergic reward pathway when ethanol and cocaine are used together; this may help to explain the high incidence of coabuse of ethanol and cocaine.
机译：乙醇和可卡因的共同滥用是最常用的药物组合之一，可导致肝脏形成可卡因乙烯。腹侧被盖区（VT A）的Oopaminergic神经元在滥用药物（包括乙醇和可卡因）的奖励特性中起关键作用。我们之前已经检查了乙醇和可卡因的电生理作用，以及它们对这些神经元的综合作用。本研究调查了可卡乙烯对多巴胺能VTA神经元的电生理作用，并在来自Fischer 344大鼠的脑切片中记录了细胞外单单位。可卡因乙烯（1-10 JLM）降低了多巴胺能VTA神经元的放电速率，类似于在此浓度范围内可卡因的作用。这种抑制被O2多巴胺受体拮抗剂sulpiride（2 JLM）阻断。浓度较低。可卡因（500 nM）增强了乙醇诱导的这些神经元的兴奋，类似于先前报道的可卡因（500 nM）的作用。 5-HT 2拮抗剂酮色林（5，LLM）逆转了古柯乙烯对乙醇激发的这种增强作用。这些数据表明，可卡乙烯通过低浓度的血清素能机制来增强乙醇对奖励神经元的兴奋，而通过高浓度的多巴胺能机制起作用。这两种作用中可可乙烯的效力与可卡因相似。当乙醇和可卡因一起使用时，可卡乙烯的这些作用可能有助于对多巴胺能奖励途径的协同作用。这可能有助于解释乙醇和可卡因共同滥用的高发生率。

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