Interleukin-1β modulates state-dependent discharge activity of preoptic area and basal forebrain neurons:: role in sleep regulation
Interleukin-1β modulates state-dependent discharge activity of preoptic area and basal forebrain neurons:: role in sleep regulation
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DOI：
10.1111/j.1460-9568.2004.03469.x
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发表时间：
2004-07-01
影响因子：
3.4
通讯作者：
Szymusiak, R
中科院分区：
文献类型：
--
作者：
Alam, MN;McGinty, D;Szymusiak, R
白细胞介素-1 β（IL-1）是一种促炎细胞因子，参与非快速眼动（nonREM）睡眠的调节。IL-1、IL-1受体和IL-1受体拮抗剂（ra）通常存在于离散的脑区域，包括下丘脑的视前区（POA）和相邻的大细胞基底前脑（BF）。POA/BF参与了睡眠-觉醒的调节。我们假设IL-1促进非REM睡眠，部分是通过改变POA/BF神经元的状态依赖性放电活动。我们记录了83个神经元的睡眠-觉醒放电曲线，并评估了IL-1，IL-1 ra，和IL-ra + IL-1通过微透析探针对状态依赖性神经元放电活动的影响。IL-1降低POA/BF神经元的放电频率，但唤醒相关和睡眠相关神经元的反应不同。IL-1显著降低唤醒相关神经元的放电频率。在24个觉醒相关神经元中，19个（79%）神经元在清醒时IL-1的存在下放电变化大于20%。IL-1抑制19个反应神经元中的18个的放电活动。在研究的13个睡眠相关神经元中，IL-1增加了5个神经元的放电活动，抑制了4个神经元的放电活动。IL-1 ra增加了9个神经元中的4个的放电活动，并显著减弱了IL-1对POA/BF神经元（n = 19）的神经元活动的诱导作用。这些结果表明，IL-1的睡眠促进作用可能是介导的，在一定程度上，通过抑制觉醒相关的神经元和激活POA/BF中的睡眠相关的神经元的亚群。
Interleukin-1beta (IL-1) is a pro-inflammatory cytokine that has been implicated in the regulation of nonrapid eye movement (nonREM) sleep. IL-1, IL-1 receptors and the IL-1 receptor antagonist (ra) are present normally in discrete brain regions, including the preoptic area (POA) of the hypothalamus and the adjoining magnocellular basal forebrain (BF). The POA/BF have been implicated in the regulation of sleep-wakefulness. We hypothesized that IL-1 promotes nonREM sleep, in part by altering the state-dependent discharge activity of POA/BF neurons. We recorded the sleep-wake discharge profiles of 83 neurons in the lateral POA/BF and assessed the effects of IL-1, IL-1ra, and IL-ra + IL-1 delivered through a microdialysis probe on state-dependent neuronal discharge activity. IL-1 decreased the discharge rate of POA/BF neurons as a group (n = 55) but wake-related and sleep-related neurons responded differently. IL-1 significantly decreased the discharge rate of wake-related neurons. Of 24 wake-related neurons studied, 19 (79%) neurons exhibited a greater than 20% change in their discharge in the presence of IL-1 during waking. IL-1 suppressed the discharge activity of 18 of 19 responsive neurons. Of 13 sleep-related neurons studied, IL-1 increased the discharge activity of five and suppressed the discharge activity of four neurons. IL-1ra increased the discharge activity of four of nine neurons and significantly attenuated IL-1-induced effects on neuronal activity of POA/BF neurons (n = 19). These results suggest that the sleep-promoting effects of IL-1 may be mediated, in part, via the suppression of wake-related neurons and the activation of a subpopulation of sleep-related neurons in the POA/BF.