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首页> 外文期刊>Addiction biology >Increased ethanol intake in prodynorphin knockout mice is associated to changes in opioid receptor function and dopamine transmission
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Increased ethanol intake in prodynorphin knockout mice is associated to changes in opioid receptor function and dopamine transmission

机译：前强啡肽敲除小鼠乙醇摄入量增加与阿片受体功能和多巴胺传递的变化有关

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The purpose of this study was to examine the role of the prodynorphin gene in alcohol sensitivity, preference and vulnerability to alcohol consumption. Handling-induced convulsion (HIC) associated to alcohol, alcohol-induced loss of righting reflex (LORR), hypothermic effects in response to acute ethanol challenge, blood ethanol levels (BELs), conditioned place preference, voluntary ethanol consumption and preference, tyrosine hydroxylase (TH), dopamine transporter (DAT) and proenkephalin (PENK) gene expression, and μ-, δ- and κ-opioid agonist-stimulated [S 35]- guanosine 5′-triphosphate-binding autoradiography were studied in prodynorphin knockout (PDYN KO) and wild-type (WT) mice. There were no differences in HIC, LORR or the decrease in body temperature in response to acute ethanol challenge between PDYN KO and WT mice. PDYN KO mice presented higher BEL, higher ethanol-conditioned place preference and more ethanol consumption and preference in a two-bottle choice paradigm than WT mice. These findings were associated with lower TH and higher DAT gene expression in the ventral tegmental area and substantia nigra, and with lower PENK gene expression in the caudate-putamen (CPu), accumbens core (AcbC) and accumbens shell (AcbSh) in PDYN KO. The functional activity of the μ-opioid receptor was lower in the CPu, AcbC, AcbSh and cingulate cortex (Cg) of PDYN KO mice. In contrast, δ- and κ-opioid receptor-binding autoradiographies were increased in the CPu and Cg (δ), and in the CPu, AcbC and Cg (κ) of PDYN KO. These results suggest that deletion of the PDYN gene increased vulnerability for ethanol consumption by altering, at least in part, PENK, TH and DAT gene expression, and μ-, δ- and κ-opioid receptor functional activity in brain areas closely related to ethanol reinforcement.
机译：这项研究的目的是检查前强啡肽基因在酒精敏感性，偏好和饮酒脆弱性中的作用。与酒精相关的处理引起的抽搐（HIC），酒精引起的恢复力丧失（LORR），对急性乙醇挑战的反应的低温效应，血液乙醇水平（BELs），条件性场所偏爱，自愿性乙醇消费和偏爱，酪氨酸羟化酶（TH），多巴胺转运蛋白（DAT）和前脑啡肽（PENK）基因表达以及μ，δ和κ阿片类激动剂刺激的[S 35]-鸟苷5'-三磷酸结合放射自显影研究了强啡肽原敲除（PDYN） KO）和野生型（WT）小鼠。 PDYN KO和WT小鼠在急性乙醇攻击后，HIC，LORR或体温下降没有差异。与WT小鼠相比，PDYN KO小鼠在两瓶选择范例中表现出更高的BEL，更高的乙醇条件位置偏好和更多的乙醇消耗及偏好。这些发现与PDYN KO腹侧被盖区和黑质中较低的TH和较高的DAT基因表达，以及与PDYN KO的尾状-丘脑（CPu），伏伏核（AcbC）和伏伏壳（AcbSh）较低的PENK基因表达有关。 。在PDYN KO小鼠的CPu，AcbC，AcbSh和扣带回皮层（Cg）中，μ阿片受体的功能活性较低。相比之下，PDyn KO的CPu和Cg（δ）以及CPu，AcbC和Cg（κ）中的δ和κ阿片受体结合放射自显影增加。这些结果表明，PDYN基因的缺失至少部分改变了PENK，TH和DAT基因的表达以及与乙醇密切相关的大脑区域的μ-，δ-和κ阿片受体功能活性，从而增加了乙醇消耗的脆弱性。加强。

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