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首页> 外文期刊>Life sciences >Chronic cocaine administration decreases the functional coupling of GABA(B) receptors in the rat ventral tegmental area as measured by baclofen-stimulated 35S-GTPgammaS binding.
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Chronic cocaine administration decreases the functional coupling of GABA(B) receptors in the rat ventral tegmental area as measured by baclofen-stimulated 35S-GTPgammaS binding.

机译：长期服用可卡因可降低大鼠腹侧被盖区中GABA（B）受体的功能偶联，如巴氯芬刺激35S-GTPgammaS结合所测。

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Results of numerous studies indicate that the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) modulates central dopamine systems, and that GABA(B) receptors may play a primary role in decreasing dopamine release. To determine if chronic cocaine administration alters the functional coupling of GABA(B) receptors to G-proteins in central dopamine systems, male F-344 rats received cocaine (15 mg/kg/injection) or saline three times a day at hourly intervals for fourteen consecutive days. Rats were decapitated one hour after the last injection and crude membrane preparations were made from the substantia nigra, caudate-putamen, ventral tegmental area, nucleus accumbens, and frontal cortex of individual rats. The ability of the specific GABA(B) receptor agonist baclofen to stimulate 35S-GTPgammaS binding in each of these regions was determined for individual animals. Additionally, baclofen-stimulated 35S-GTPgammaS binding in each of these regions in rats that received cocaine was compared to baclofen-stimulated 35S-GTPgammaS binding in rats that received control injections of saline. The EC50 of baclofen and maximal baclofen-stimulated 35S-GTPgammaS binding over basal levels were determined in each brain region in the saline group and in the cocaine group. Two-way ANOVA revealed a significant decrease in GABA(B) receptor-stimulated 35S-GTPgammaS binding in the ventral tegmental area of the cocaine group compared to the saline group. These data suggest that chronic exposure to cocaine decreases the functional coupling of GABA(B) receptors to G-proteins selectively in the ventral tegmental area. This finding may have implications in the augmented extracellular dopamine levels seen in the nucleus accumbens of rats that have been sensitized to cocaine.
机译：大量研究结果表明，抑制性神经递质γ-氨基丁酸（GABA）调节中枢多巴胺系统，并且GABA（B）受体可能在减少多巴胺释放中起主要作用。为了确定长期服用可卡因是否会改变GABA（B）受体与中枢多巴胺系统中G蛋白的功能偶联，雄性F-344大鼠每天隔三小时每天接受三次可卡因（15 mg / kg /注射）或生理盐水，连续十四天。最后一次注射后一小时，将大鼠断头，并从黑质，尾状-丘脑，腹侧被盖区，伏隔核和额叶皮层制备粗制膜。对于个别动物，确定了特异性GABA（B）受体激动剂巴氯芬在这些区域的每一个中刺激35S-GTPγS结合的能力。另外，将接受可卡因的大鼠中每个区域中巴氯芬刺激的35S-GTPgammaS结合与接受对照注射盐水的大鼠中对巴氯芬刺激的35S-GTPgammaS结合进行了比较。在盐水组和可卡因组的每个脑区域中测定了巴氯芬的EC50和巴氯芬刺激的最大35S-GTPgammaS在基础水平上的结合。双向方差分析显示，与盐水组相比，可卡因组腹侧被盖区中GABA（B）受体刺激的35S-GTPgammaS结合显着降低。这些数据表明，长期暴露于可卡因会降低腹侧被盖区中GABA（B）受体与G蛋白的功能偶联。这一发现可能与对可卡因致敏的大鼠伏隔核中细胞外多巴胺水平升高有关。

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