Leptin excites basolateral amygdala principal neurons and reduces food intake by LepRb-JAK2-PI3K-dependent depression of GIRK channels,Journal of Cellular Physiology

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Leptin excites basolateral amygdala principal neurons and reduces food intake by LepRb-JAK2-PI3K-dependent depression of GIRK channels
Journal of Cellular Physiology ( IF 4.5 ) Pub Date : 2023-09-08 , DOI: 10.1002/jcp.31117
Cody A Boyle ₁ , Phani K Kola ₁ , Chidiebele S Oraegbuna ₁ , Saobo Lei ₁

Affiliation

Leptin is an adipocyte-derived hormone that modulates food intake, energy balance, neuroendocrine status, thermogenesis, and cognition. Whereas a high density of leptin receptors has been detected in the basolateral amygdala (BLA) neurons, the physiological functions of leptin in the BLA have not been determined yet. We found that application of leptin excited BLA principal neurons by activation of the long form leptin receptor, LepRb. The LepRb-elicited excitation of BLA neurons was mediated by depression of the G protein-activated inwardly rectifying potassium (GIRK) channels. Janus Kinase 2 (JAK2) and phosphoinositide 3-kinase (PI3K) were required for leptin-induced excitation of BLA neurons and depression of GIRK channels. Microinjection of leptin into the BLA reduced food intake via activation of LepRb, JAK2, and PI3K. Our results may provide a cellular and molecular mechanism to explain the physiological roles of leptin in vivo.

中文翻译：

瘦素通过 LepRb-JAK2-PI3K 依赖性 GIRK 通道抑制来兴奋基底外侧杏仁核主要神经元并减少食物摄入

瘦素是一种脂肪细胞衍生的激素，可调节食物摄入、能量平衡、神经内分泌状态、产热和认知。虽然在基底外侧杏仁核 (BLA) 神经元中检测到高密度的瘦素受体，但 BLA 中瘦素的生理功能尚未确定。我们发现瘦素的应用通过激活长型瘦素受体 LepRb 来兴奋 BLA 主要神经元。 LepRb 引起的 BLA 神经元兴奋是通过抑制 G 蛋白激活的内向整流钾 (GIRK) 通道介导的。 Janus 激酶 2 (JAK2) 和磷酸肌醇 3-激酶 (PI3K) 是瘦素诱导的 BLA 神经元兴奋和 GIRK 通道抑制所必需的。将瘦素显微注射到 BLA 中可通过激活 LepRb、JAK2 和 PI3K 来减少食物摄入。我们的结果可能提供细胞和分子机制来解释瘦素在体内的生理作用。

更新日期：2023-09-08

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