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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Inhibition by ginsenosides Rb1 and Rg1 of cocaine-induced hyperactivity, conditioned place preference, and postsynaptic dopamine receptor supersensitivity in mice.
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Inhibition by ginsenosides Rb1 and Rg1 of cocaine-induced hyperactivity, conditioned place preference, and postsynaptic dopamine receptor supersensitivity in mice.

机译：人参皂甙Rb1和Rg1对可卡因诱导的过度活跃，条件性位置偏爱和突触后多巴胺受体超敏性的抑制作用。

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摘要

A single or repeated administration of cocaine (15 mg/kg) in mice produced hyperactivity and conditioned place preference (CPP). Ginsenoside Rb1 (Rb1) and ginsenoside Rg1 (Rg1), prior to and during the cocaine treatment in mice, inhibited cocaine-induced hyperactivity and CPP. The development of enhanced postsynaptic dopamine (DA) receptor sensitivity in mice displaying a cocaine-induced CPP was evidenced by the enhanced response in ambulatory activity to the DA agonist, apomorphine (2 mg/kg). Rb1 and Rg1 inhibited the development of postsynaptic DA receptor supersensitivity. However, Rb1 and Rg1 did not show any antidopaminergic activity at the postsynaptic DA receptors, because the apomorphine-induced climbing behavior was not inhibited by Rb1 and Rg1. Therefore, it is presumed that Rb1 and Rg1 modulate DA activity induced by cocaine at the presynaptic DA receptors, and this modulation results in the inhibition of postsynaptic dopaminergic activation. These results suggest that the cocaine-induced CPP may be associated with enhanced DA receptor sensitivity. The inhibition by Rb1 and Rg1 of cocaine-induced hyperactivity and CPP may be closely related with the inhibition of dopaminergic activation induced by cocaine at the presynaptic DA receptors.
机译：在小鼠中单次或重复施用可卡因（15 mg / kg）会产生活动过度和条件性位置偏爱（CPP）。人参皂苷Rb1（Rb1）和人参皂苷Rg1（Rg1），在小鼠中可卡因治疗之前和之中，抑制了可卡因诱导的机能亢进和CPP。表现出可卡因诱导的CPP的小鼠突触后多巴胺（DA）受体敏感性的增强可以通过对DA激动剂阿扑吗啡（2 mg / kg）的活动能力增强来证明。 Rb1和Rg1抑制突触后DA受体超敏性的发展。但是，Rb1和Rg1在突触后DA受体上没有显示任何抗多巴胺能活性，因为阿扑吗啡诱导的爬升行为不受Rb1和Rg1抑制。因此，推测Rb1和Rg1调节可卡因在突触前DA受体上诱导的DA活性，并且这种调节导致突触​​后多巴胺能激活的抑制。这些结果表明可卡因诱导的CPP可能与DA受体敏感性增强有关。 Rb1和Rg1对可卡因诱导的过度活跃和CPP的抑制作用可能与可卡因对突触前DA受体诱导的多巴胺能激活的抑制作用密切相关。

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