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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Ghrelin amplifies the nicotine-induced dopamine release in the rat striatum
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Ghrelin amplifies the nicotine-induced dopamine release in the rat striatum

机译：Ghrelin放大尼古丁引起的大鼠纹状体中多巴胺的释放

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The orexigenic peptide ghrelin plays a prominent role in the regulation of energy balance and in the mediation of reward mechanisms and reinforcement for addictive drugs, such as nicotine. Nicotine is the principal psychoactive component in tobacco, which is responsible for addiction and relapse of smokers. Nicotine activates the mesencephalic dopaminergic neurons via nicotinic acetylcholine receptors (nAchR). Ghrelin stimulates the dopaminergic neurons via growth hormone secretagogue receptors (GHS-R1A) in the ventral tegmental area and the substantia nigra pars compacta resulting in the release of dopamine in the ventral and dorsal striatum, respectively. In the present study an in vitro superfusion of rat striatal slices was performed, in order to investigate the direct action of ghrelin on the striatal dopamine release and the interaction of ghrelin with nicotine through this neurotransmitter release. Ghrelin increased significantly the dopamine release from the rat striatum following electrical stimulation. This stimulatory effect was reversed by both the selective nAchR antagonist mecamylamine and the selective GHS-R1A antagonist GHRP-6. Nicotine also increased significantly the dopamine release under the same conditions. This stimulatory effect was antagonized by mecamylamine, but not by GHRP-6. Ghrelin further stimulated the nicotine-induced dopamine release and this effect was abolished by mecamylamine and was partially inhibited by GHRP-6. The present results demonstrate that ghrelin stimulates directly the dopamine release and amplifies the nicotine-induced dopamine release in the rat striatum. We presume that striatal cholinergic interneurons also express GHS-R1A, through which ghrelin can amplify the nicotine-induced dopamine release in the striatum. This study provides further evidence of the impact of ghrelin on the mesolimbic and nigrostriatal dopaminergic pathways. It also suggests that ghrelin signaling may serve as a novel pharmacological target for treatment of addictive and neurodegenerative disorders.
机译：致食性肽生长激素释放肽在调节能量平衡，奖励机制和增强尼古丁等成瘾性药物方面起着重要作用。尼古丁是烟草中的主要精神活性成分，负责吸烟者的成瘾和复发。尼古丁通过烟碱乙酰胆碱受体（nAchR）激活中脑多巴胺能神经元。 Ghrelin通过腹侧被盖区和黑质致密部中的生长激素促分泌素受体（GHS-R1A）刺激多巴胺能神经元，分别在腹侧和背侧纹状体中释放多巴胺。在本研究中，进行了大鼠纹状体切片的体外灌注，以研究ghrelin对纹状体多巴胺释放的直接作用以及ghrelin与尼古丁通过这种神经递质释放的相互作用。 Ghrelin在电刺激后显着增加了大鼠纹状体中多巴胺的释放。选择性nAchR拮抗剂美加明胺和选择性GHS-R1A拮抗剂GHRP-6均逆转了这种刺激作用。在相同条件下，尼古丁还显着增加了多巴胺的释放。美甲胺可拮抗这种刺激作用，而GHRP-6则不能。 Ghrelin进一步刺激了尼古丁诱导的多巴胺释放，美卡敏消除了该作用，GHRP-6则部分抑制了该作用。目前的结果表明，生长素释放肽直接刺激多巴胺的释放，并放大了大鼠纹状体中烟碱诱导的多巴胺的释放。我们推测纹状体胆碱能中间神经元也表达GHS-R1A，ghrelin可以通过GHS-R1A放大尼古丁引起的纹状体中多巴胺的释放。这项研究提供了ghrelin对中脑边缘和黑质纹状体多巴胺能途径的影响的进一步证据。这也表明ghrelin信号传导可以作为治疗成瘾性和神经退行性疾病的新型药理靶标。

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