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首页> 外文期刊>Molecular Metabolism >Astroglial CB'1 cannabinoid receptors regulate leptin signaling in mouse brain astrocytes
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Astroglial CB'1 cannabinoid receptors regulate leptin signaling in mouse brain astrocytes

机译：星形胶质细胞CB“ 1大麻素受体调节小鼠脑星形胶质细胞中的瘦素信号传导

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Type-1 cannabinoid (CB"1) and leptin (ObR) receptors regulate metabolic and astroglial functions, but the potential links between the two systems in astrocytes were not investigated so far. Genetic and pharmacological manipulations of CB"1 receptor expression and activity in cultured cortical and hypothalamic astrocytes demonstrated that cannabinoid signaling controls the levels of ObR expression. Lack of CB"1 receptors also markedly impaired leptin-mediated activation of signal transducers and activators of transcription 3 and 5 (STAT3 and STAT5) in astrocytes. In particular, CB"1 deletion determined a basal overactivation of STAT5, thereby leading to the downregulation of ObR expression, and leptin failed to regulate STAT5-dependent glycogen storage in the absence of CB"1 receptors. These results show that CB"1 receptors directly interfere with leptin signaling and its ability to regulate glycogen storage, thereby representing a novel mechanism linking endocannabinoid and leptin signaling in the regulation of brain energy storage and neuronal functions.
机译：1型大麻素（CB“ 1）和瘦蛋白（ObR）受体调节代谢和星形胶质细胞的功能，但到目前为止，尚未研究星形胶质细胞中这两个系统之间的潜在联系。CB” 1受体表达和活性的遗传和药理学操作培养的皮质和下丘脑星形胶质细胞证明大麻素信号传导控制ObR表达水平。 CB“ 1受体的缺乏也显着损害了星形胶质细胞中瘦素介导的瘦素介导的信号转导子和转录3和5激活子（STAT3和STAT5）的激活。特别是，CB” 1缺失决定了STAT5的基础过度激活，从而导致了STAT5的下调。在没有CB“ 1受体的情况下，瘦素无法调节STAT5依赖性糖原存储。这些结果表明，CB” 1受体直接干扰瘦素信号传导及其调节糖原存储的能力，从而代表了一种新的机制内源性大麻素和瘦素信号传导在调节脑能量储存和神经元功能中的作用。

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