Input organization and plasticity of hypocretin neurons: Possible clues to obesity's association with insomnia
Input organization and plasticity of hypocretin neurons: Possible clues to obesity's association with insomnia
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DOI：
10.1016/j.cmet.2005.03.003
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发表时间：
2005-04-01
期刊：
影响因子：
29
通讯作者：
Gao, XB
中科院分区：
文献类型：
--
作者：
Horvath, TL;Gao, XB
下丘脑外侧下丘脑(也称为增食欲素)神经元在激发觉醒和调节能量代谢方面发挥着重要作用。缺乏下丘脑泌素信号是发作性睡病的原因，而下丘脑生长素水平升高则会导致觉醒、食物摄入量增加和肥胖。在这里，我们报告了一种非正统的突触组织，在下丘脑神经元上，兴奋性突触电流和不对称突触以最小的抑制输入控制这些长投射神经元的胞体。过夜的食物剥夺促进了更多兴奋性突触和突触电流的形成，这些突触电流通过重新进食而逆转，并被瘦素注射阻断。这种独特的连接和应激诱导的下丘脑神经元的可塑性与它们参与对生存至关重要的觉醒和警觉的控制很好地相关，但这种回路也可能是失眠和相关代谢障碍的潜在原因，包括肥胖。
The lateral hypothalamic hypocretin (also called orexin) neurons have emerged as instrumental in triggering arousal and regulating energy metabolism. The lack of hypocretin signaling is the cause of narcolepsy while elevated hypocretin levels induce arousal, elevated food intake, and adiposity. Here, we report an unorthodox synaptic organization on the hypocretin neurons in which excitatory synaptic currents and asymmetric synapses exert control on the cell bodies of these long-projective neurons with minimal inhibitory input. Overnight food deprivation promotes the formation of more excitatory synapses and synaptic currents onto hypocretin cells; this is reversed by re-feeding and blocked by leptin administration. This unique wiring and acute stress-induced plasticity of the hypocretin neurons correlates well with their being involved in the control of arousal and alertness that are so vital to survival, but this circuitry may also be an underlying cause of insomnia and associated metabolic disturbances, including obesity.