Leptin-inhibited neurons in the lateral parabrachial nucleus do not alter food intake or glucose balance.
Leptin-inhibited neurons in the lateral parabrachial nucleus do not alter food intake or glucose balance.
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DOI：
10.1080/19768354.2022.2084159
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发表时间：
2022
影响因子：
2.9
通讯作者：
Sohn, Jong Woo
中科院分区：
文献类型：
--
作者：
Park, Seahyung;Williams, Kevin W.;Sohn, Jong Woo
臂旁外侧核（LPBN）在药理学、光遗传学和化学发生学水平上参与食欲抑制。然而，在生理条件下介导这些神经元激活的信号传导受到难以分离该区域不同细胞群的阻碍。使用报告小鼠，我们确定在电生理水平上的影响，肾上腺素激素，瘦素，在LPBN（LPBNObR神经元）的瘦素受体（ObR）表达的神经元。瘦素的应用导致LPBNObR神经元亚群的抑制。这种作用是介导的增加钾电导，也伴随着减少兴奋性突触输入到这些神经元。然而，通过化学遗传学模拟瘦素对LPBNObR神经元的抑制作用导致摄食或葡萄糖水平没有变化，这表明瘦素对LPBNObR神经元的作用可能不足以调节这些代谢方面。
The lateral parabrachial nucleus (LPBN) has been shown to be involved in the suppression of appetite at the pharmacological, optogenetic and chemogenetic levels. However, the signalling that mediates activation of these neurons in physiological conditions has been hindered by difficulties in segregating different cell populations in this region. Using reporter mice, we identify at the electrophysiological level the effects of an anorexic hormone, leptin, on leptin receptor (ObR)-expressing neurons in the LPBN (LPBNObR neurons). Application of leptin caused inhibition in a subpopulation of LPBNObR neurons. This effect was mediated by an increased potassium conductance and was also accompanied by a decrease in excitatory synaptic input onto these neurons. However, mimicking the inhibitory effects of leptin on LPBNObR neurons through chemogenetics led to no changes in feeding or glucose levels, which suggests that leptin action on LPBNObR neurons may not be sufficient to regulate these metabolic aspects.