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首页> 外文期刊>The European Journal of Neuroscience >Interleukin-1beta enhances non-rapid eye movement sleep when microinjected into the dorsal raphe nucleus and inhibits serotonergic neurons in vitro.
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Interleukin-1beta enhances non-rapid eye movement sleep when microinjected into the dorsal raphe nucleus and inhibits serotonergic neurons in vitro.

机译：白细胞介素-1β显微注射到背缝核后可增强非快速眼动睡眠，并在体外抑制血清素能神经元。

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摘要

Interleukin-1 (IL-1) and IL-1 receptors are constitutively expressed in normal brain. IL-1 increases non-rapid eye movements (NREM) sleep in several animal species, an effect mediated in part by interactions with the serotonergic system. The site(s) in brain at which interactions between IL-1 and the serotonergic system increase NREM sleep remain to be identified. The dorsal raphe (DRN) is the origin of the major ascending serotonergic pathways to the forebrain, and it contains IL-1 receptors. This study examined the hypothesis that IL-1 increases NREM sleep by acting at the level of the DRN. IL-1beta (0.25 and 0.5 ng) was microinjected into the DRN of freely behaving rats and subsequent effects on sleep-wake activity were determined. IL-1beta 0.5 ng increased NREM sleep during the first 2 h post-injection from 33.5 +/- 3.7% after vehicle microinjection to 42.9 +/- 3.0% of recording time. To determine the effects of IL-1beta on electrophysiological properties of DRN serotonergic neurons, intracellular recordings were performed in a guinea-pig brain stem slice preparation. In 26 of 32 physiologically and pharmacologically identified serotonergic neurons, IL-1beta superfusion (25 ng/mL) decreased spontaneous firing rates by 50%, from 1.6 +/- 0.2 Hz (before IL-1beta superfusion) to 0.8 +/- 0.2 Hz. This effect was reversible upon washout. These results show that IL-1beta increases NREM sleep when administered directly into the DRN. Serotonin enhances wakefulness and these novel data also suggest that IL-1beta-induced enhancement of NREM sleep could be due in part to the inhibition of DRN serotonergic neurons.
机译：白细胞介素-1（IL-1）和IL-1受体在正常大脑中组成性表达。 IL-1增加了几种动物的非快速眼动（NREM）睡眠，这种作用部分是通过与血清素能系统的相互作用介导的。 IL-1和血清素能系统之间的相互作用会增加NREM睡眠的大脑部位尚待确定。背缝（DRN）是通往前脑的主要上升血清素能途径的起源，它含有IL-1受体。这项研究检验了IL-1通过在DRN水平上起作用来增加NREM睡眠的假设。将IL-1beta（0.25和0.5 ng）微注射到行为自由的大鼠的DRN中，然后测定其对睡眠-唤醒活动的影响。 IL-1beta 0.5 ng可使注射后最初2 h的NREM睡眠时间从媒介物微量注射后的33.5 +/- 3.7％增加到记录时间的42.9 +/- 3.0％。为了确定IL-1β对DRN血清素能神经元电生理特性的影响，在豚鼠脑干切片制剂中进行了细胞内记录。在32种生理和药理学鉴定的血清素能神经元中的26种中，IL-1beta融合（25 ng / mL）使自发放电率降低了50％，从1.6 +/- 0.2 Hz（在IL-1beta融合之前）降至0.8 +/- 0.2 Hz 。冲洗后这种作用是可逆的。这些结果表明，当直接施用到DRN中时，IL-1beta可增加NREM睡眠。血清素可增强清醒作用，这些新数据还表明，IL-1β诱导的NREM睡眠增强可能部分归因于DRN血清素能神经元的抑制。

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