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首页> 外文期刊>The European Journal of Neuroscience >Effects of hypocretin (orexin) neuronal loss on sleep and extracellular adenosine levels in the rat basal forebrain.
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Effects of hypocretin (orexin) neuronal loss on sleep and extracellular adenosine levels in the rat basal forebrain.

机译：降钙素（orexin）神经元丢失对大鼠基底前脑的睡眠和细胞外腺苷水平的影响。

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Neurons containing the neuropeptide hypocretin (HCRT, orexin) are localized only in the lateral hypothalamus, from where they innervate multiple regions implicated in arousal, including the basal forebrain. HCRT activation of downstream arousal neurons is likely to stimulate release of endogenous factors. One such factor is adenosine, which in the basal forebrain increases in level with wakefulness and decreases with sleep, and is hypothesized to regulate the waxing and waning of sleep drive. Does loss of HCRT neurons affect adenosine levels in the basal forebrain? Is the increased sleep that accompanies HCRT loss a consequence of higher adenosine levels in the basal forebrain? In the present study, we investigated these questions by lesioning the HCRT neurons with HCRT-2-saporin (HCRT-2-SAP) and measuring sleep and extracellular levels of adenosine in the basal forebrain. In separate groups of rats, the neurotoxin HCRT-2-SAP or saline was administered locally to the lateral hypothalamus, and 80 days later adenosine and sleep were assessed. Rats given the neurotoxin had a 94% loss of HCRT neurons. These rats woke less at night, and had more rapid eye movement sleep, which is consistent with HCRT hypofunction. These rats also had more sleep after brief periods of sleep deprivation. However, in the lesioned rats, adenosine levels did not increase with 6 h of sleep deprivation, whereas an increase in adenosine levels occurred in rats without lesion of the HCRT neurons. These findings indicate that adenosine levels do not increase with wakefulness in rats with a HCRT lesion, and that the increased sleep in these rats occurs independently of adenosine levels in the basal forebrain.
机译：含有神经肽降钙素（HCRT，orexin）的神经元仅位于下丘脑外侧，从中支配涉及唤醒的多个区域，包括基底前脑。下游唤醒神经元的HCRT激活可能会刺激内源性因子的释放。一种这样的因子是腺苷，其在前脑的基础上随着觉醒而增加水平，并随着睡眠而降低，并且被认为可以调节睡眠驱动的增加和减少。 HCRT神经元丢失会影响基底前脑中的腺苷水平吗？伴随HCRT丧失而增加的睡眠是否是基底前脑中较高的腺苷水平导致的？在本研究中，我们通过用HCRT-2-saporin（HCRT-2-SAP）破坏HCRT神经元并测量基底前脑的睡眠和腺苷的细胞外水平来调查这些问题。在单独的大鼠组中，将神经毒素HCRT-2-SAP或生理盐水局部施用于下丘脑外侧，并在80天后评估腺苷和睡眠。服用神经毒素的大鼠的HCRT神经元损失了94％。这些大鼠夜间醒得更少，并且眼动运动睡眠更快，这与HCRT功能低下是一致的。在短暂的睡眠剥夺之后，这些大鼠也有更多的睡眠。然而，在患病大鼠中，腺苷水平并未随睡眠剥夺6小时而增加，而在没有HCRT神经元病变的大鼠中，腺苷水平却升高。这些发现表明，在患有HCRT病变的大鼠中，腺苷水平不会随着觉醒而增加，并且这些大鼠的睡眠增加与基底前脑中的腺苷水平无关。

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