促肾上腺皮质激素原3基因敲除小鼠的酒精摄入量增加不受慢性炎性疼痛的影响。
Increased alcohol consumption in urocortin 3 knockout mice is unaffected by chronic inflammatory pain.
作者信息
Smith Monique L, Li Ju, Ryabinin Andrey E
机构信息
Department of Behavioral Neuroscience, Oregon Health & Science University, 3181 SW Sam Jackson Park Road L470, Portland, OR 97239-3098, USA.
Department of Behavioral Neuroscience, Oregon Health & Science University, 3181 SW Sam Jackson Park Road L470, Portland, OR 97239-3098, USA
出版信息
Alcohol Alcohol. 2015 Mar;50(2):132-9. doi: 10.1093/alcalc/agu084. Epub 2014 Dec 1.
AIMS
Stress neurocircuitry may modulate the relationship between alcohol drinking and chronic pain. The corticotropin-releasing factor (CRF) system is crucial for regulation of stress responses. The current study aimed to elucidate the role of the endogenous CRF ligand Urocortin 3 (Ucn3) in the relationship between alcohol drinking behavior and chronic pain using a genetic approach.
METHODS
Ucn3 (KO) and wildtype (WT) littermates were subjected to a 24-h access drinking procedure prior to and following induction of chronic inflammatory pain.
RESULTS
Ucn3 KO mice displayed significantly increased ethanol intake and preference compared with WT across the time course. There were no long-term effects of chronic pain on alcohol drinking behavior, regardless of genotype, nor any evidence for alcohol-induced analgesia.
CONCLUSION
The increased drinking in Ucn3 KO supports a role for this peptide in alcohol-related behavior. These data suggest the necessity for more research exploring the relationship between alcohol drinking, chronic pain and the CRF system in rodent models.
目的
应激神经回路可能调节饮酒与慢性疼痛之间的关系。促肾上腺皮质激素释放因子（CRF）系统对调节应激反应至关重要。本研究旨在采用遗传学方法阐明内源性CRF配体尿皮质素3（Ucn3）在饮酒行为与慢性疼痛关系中的作用。
方法
在诱导慢性炎性疼痛之前和之后，对Ucn3基因敲除（KO）小鼠和野生型（WT）同窝小鼠进行24小时自由饮用酒精实验。
结果
在整个实验过程中，与野生型小鼠相比，Ucn3基因敲除小鼠的乙醇摄入量和偏好显著增加。无论基因型如何，慢性疼痛对饮酒行为均无长期影响，也没有酒精诱导镇痛的证据。
结论
Ucn3基因敲除小鼠饮酒量增加，表明该肽在与酒精相关的行为中发挥作用。这些数据表明，有必要在啮齿动物模型中开展更多研究，以探索饮酒、慢性疼痛和CRF系统之间的关系。
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