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首页> 外文期刊>The European Journal of Neuroscience >Cocaine-induced locomotor activity and Fos expression in nucleus accumbens are sensitized for 6 months after repeated cocaine administration outside the home cage.
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Cocaine-induced locomotor activity and Fos expression in nucleus accumbens are sensitized for 6 months after repeated cocaine administration outside the home cage.

机译：可卡因诱导的自发活动和伏隔核中的Fos表达在家庭笼子外重复施用可卡因后6个月敏感。

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摘要

Induction of the immediate early gene protein product Fos has been used extensively to assess neural activation in the striatum after repeated cocaine administration to rats in their home cages but rarely after repeated administration outside the home cage, which produces more robust locomotor sensitization. In the present study, we found cocaine-induced Fos expression in nucleus accumbens, but not caudate-putamen, was enhanced 1 and 6 months after repeated drug administration in locomotor activity chambers. Double-labelling of Fos protein and enkephalin mRNA indicated that Fos expression in nucleus accumbens was enhanced in enkephalin-positive, but not enkephalin-negative, medium spiny neurons. In contrast, cocaine-induced Fos expression was absent altogether in nucleus accumbens and unaltered in caudate-putamen 1 month after repeated cocaine administration in the home cage. As cocaine-induced locomotor activity was also enhanced 1 and 6 months after repeated cocaine administration in locomotor activity chambers, we wanted to confirm that neuronal activity in nucleus accumbens mediates cocaine-induced locomotor activity using our particular treatment regimen. Bilateral infusions of the GABA agonists baclofen and muscimol (1 microg/side) into nucleus accumbens of sensitized rats blocked cocaine-induced Fos expression and locomotor activity. Thus, while neuronal activity in both D1- and D2-type neurons in nucleus accumbens can mediate acute cocaine-induced locomotor activity, the enhanced activation of enkephalinergic D2-type neurons suggests that these latter neurons mediate the enhancement of cocaine-induced locomotor activity for up to 6 months after repeated drug administration outside the home cage.
机译：立即向早期基因蛋白产物Fos的诱导已广泛用于评估可卡因在其家笼中对大鼠的重复给药后纹状体中的神经激活，但很少在家笼外重复给药后产生更强的运动敏化作用。在本研究中，我们发现可卡因诱导的伏安核表达在伏隔核中增强，但在尾部活动腔中重复给药1和6个月后，尾状-丘脑则没有增强。 Fos蛋白和脑啡肽mRNA的双重标记表明伏伏核中伏脑表达在脑啡肽阳性而不是脑啡肽阴性的中等棘神经元中增强。相比之下，可卡因诱导的Fos表达在伏隔核中完全不存在，而在尾笼中重复施用可卡因后1个月，尾状壳-丘脑中的Fos表达没有改变。由于可卡因诱导的运动功能在运动活动室中重复施用可卡因后1和6个月也得到增强，因此我们想确认伏隔核中的神经元活性使用我们的特殊治疗方案介导了可卡因诱导的运动活动。 GABA激动剂巴氯芬和麝香酚（1微克/侧）的双边输注到敏化大鼠伏伏核中，阻断了可卡因诱导的Fos表达和运动能力。因此，尽管伏隔核中D1和D2型神经元的神经元活性都可以介导可卡因诱导的自发运动活性，但脑啡肽能D2型神经元的活化增强表明这些后神经元介导了可卡因诱导的自发运动在笼子外重复给药后长达6个月。

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