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自愿饮酒与慢性给予左乙拉西坦的酒精偏爱大鼠的血浆β-内啡肽水平:一项初步研究。

Voluntary alcohol consumption and plasma beta-endorphin levels in alcohol preferring rats chronically treated with levetiracetam: a preliminary study.

机构信息

Department of Pharmacodynamics, Medical University of Lodz, Muszynskiego 1, PL 90-151 Lodz, Poland.

出版信息

Physiol Behav. 2011 Mar 28;102(5):538-41. doi: 10.1016/j.physbeh.2010.12.021. Epub 2010 Dec 25.

DOI:10.1016/j.physbeh.2010.12.021
PMID:21187108
Abstract

Many recent researches have confirmed the effectiveness of antiepileptic drugs in preventing alcohol dependency, whereas our previous study showed that repeated treatment with topiramate, a new antiepileptic drug, was effective in increasing the plasma levels of beta-endorphin (an endogenous opioid peptide) in rats. It is well documented that in humans a genetic deficit of beta-endorphin is often associated with alcohol addiction as alcohol consumption elevates the level of this peptide. The aim of the present study is multifaceted: to investigate the effect of repeated treatment of levetiracetam (50 or 100mg/kg b.w., twice daily) on voluntary alcohol intake in alcohol preferring rats (Warsaw High Preferring; WHP) and to assess changes in plasma beta-endorphin levels while alcohol is available and when it is not available for an extended period of time. We observed a noticeable increase in the levels of beta-endorphin in rats with free access to alcohol whether in a prolonged levetiracetam-treated or vehicle-treated group. However, in the levetiracetam group, a voluntary intake of alcohol diminished in comparison with both the pretreatment period and in comparison with the vehicle-treated rats. A similar increase in the plasma beta-endorphin levels was observed in levetiracetam-treated rats that did not have access to ethanol. This finding lets us to believe that levetiracetam may be a promising medication in treatment of alcohol dependency as its application leads to the increase in the beta-endorphin concentration and ultimately results in reducing deficiency of this peptide.

摘要

许多最近的研究证实了抗癫痫药物在预防酒精依赖方面的有效性,而我们之前的研究表明,反复使用新型抗癫痫药物托吡酯可有效增加大鼠血浆β-内啡肽(一种内源性阿片肽)的水平。有充分的文献记载表明,在人类中,β-内啡肽的遗传缺陷常常与酒精成瘾有关,因为饮酒会提高这种肽的水平。本研究的目的是多方面的:研究反复给予左乙拉西坦(50 或 100mg/kg b.w.,每日两次)对酒精偏好大鼠(华沙高偏好;WHP)自愿饮酒的影响,并评估在有和没有可延长时间的酒精时血浆β-内啡肽水平的变化。我们观察到,无论在长期左乙拉西坦治疗组还是载体治疗组,有自由接触酒精的大鼠β-内啡肽水平明显升高。然而,与治疗前时期和载体治疗大鼠相比,左乙拉西坦组大鼠的酒精自愿摄入量减少。在没有接触乙醇的左乙拉西坦治疗大鼠中也观察到血浆β-内啡肽水平的类似增加。这一发现使我们相信,左乙拉西坦可能是治疗酒精依赖的一种有前途的药物,因为它的应用会导致β-内啡肽浓度的增加,最终导致这种肽的缺乏得到缓解。

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