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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Alcohol intake of P rats is regulated by muscarinic receptors in the pedunculopontine nucleus and VTA.
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Alcohol intake of P rats is regulated by muscarinic receptors in the pedunculopontine nucleus and VTA.

机译：P大鼠的饮酒量受小足足突核和VTA中毒蕈碱受体的调节。

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Experiments were conducted to determine whether muscarinic receptors within the pedunculopontine nucleus (PPN) and ventral tegmental area (VTA) are involved in regulating ethanol drinking behavior in the alcohol-preferring P line of rats. Female P rats were given limited access (2 h/day) to 10% (v/v) ethanol and 0.0125% (g/100 ml) saccharin solutions. Food was available ad libitum. Cholinergic agents were microinjected unilaterally into the PPN or VTA immediately prior to ethanol access. Intra-PPN carbachol (1-4 microg/0.5 microl), which can inhibit cholinergic neuronal activity within the PPN, decreased ethanol (70% decrease at the highest dose; p < 0.05) and saccharin (90% decrease at the highest dose; p < 0.05) intake in a dose-dependent manner within the first 30 min. Intra-PPN scopolamine (5-15 microg/0.5 microl), which can stimulate cholinergic neuronal activity within the PPN, decreased ethanol intake in a dose-dependent manner within the first 30 min (65% decrease at the highest dose; p < 0.05)without reducing saccharin intake. Intra-VTA methylscopolamine (1-10 microg/0.5 microl), a muscarinic antagonist, significantly (p < 0.05) reduced ethanol (60% decrease at the highest dose) and saccharin (50% decrease at the highest dose) intakes during the 2-h access period. Intra-VTA carbachol, a cholinergic agonist (1 and 2 microg/0.5 microl) decreased ethanol consumption in a dose-dependent manner within the first 60 min (50% decrease at the highest dose) without reducing saccharin intake. Overall, these results support an involvement of the cholinergic PPN-VTA system in regulating alcohol drinking and general consummatory behaviors of the P line of rats.
机译：进行了实验，以确定足小腿骨桥骨核（PPN）和腹侧被盖区（VTA）中的毒蕈碱受体是否参与了对酒精偏爱的P系大鼠的乙醇饮用行为的调节。给雌性P大鼠以有限的途径（2小时/天）使用10％（v / v）乙醇和0.0125％（g / 100ml）糖精溶液。随意提供食物。在接近乙醇之前，将胆碱能药物单侧微注射到PPN或VTA中。可抑制PPN内胆碱能神经元活性的PPN内卡巴胆碱（1-4微克/0.5微升），乙醇（最高剂量下降低70％; p <0.05）和糖精（最高剂量下降低90％）， p <0.05）在头30分钟内以剂量依赖性方式摄入。可以刺激PPN内胆碱能神经元活性的PPN内东pol碱（5-15微克/0.5微升）在前30分钟内以剂量依赖性方式减少乙醇摄入（最高剂量下减少65％; p <0.05 ），而不减少糖精的摄入量。毒蕈碱拮抗剂VTA内甲基东pol碱（1-10微克/0.5微升）在2期间的摄入量显着降低（p <0.05）乙醇（最高剂量降低60％）和糖精（最高剂量降低50％） -h访问期。 VTA内胆碱能激动剂（1和2微克/0.5微升）卡巴胆碱在最初的60分钟内以剂量依赖的方式减少了乙醇消耗（最高剂量下减少了50％），而没有减少糖精的摄入。总的来说，这些结果支持胆碱能PPN-VTA系统参与调节大鼠P系的饮酒和一般消费行为。

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