Chronic sleep restriction elevates brain interleukin-1 beta and tumor necrosis factor-alpha and attenuates brain-derived neurotrophic factor expression.
Chronic sleep restriction elevates brain interleukin-1 beta and tumor necrosis factor-alpha and attenuates brain-derived neurotrophic factor expression.
复制标题
DOI：
10.1016/j.neulet.2014.07.043
复制
发表时间：
2014-09-19
影响因子：
2.5
通讯作者：
Gerashchenko D
中科院分区：
文献类型：
--
作者：
Zielinski MR;Kim Y;Karpova SA;McCarley RW;Strecker RE;Gerashchenko D
急性睡眠不足会增加大脑中的促炎和突触可塑性相关分子，包括白细胞介素-1 β（IL-1β）、肿瘤坏死因子-α（TNF-α）和脑源性神经营养因子（BDNF）。这些分子增强非快速眼动睡眠慢波活动（SWA），也称为脑电图δ功率，并调节神经认知性能。有证据表明，慢性睡眠限制（CSR）是当今社会普遍存在的一种情况，不会引起急性睡眠不足后所见的SWA增强，尽管它会累积损害神经认知功能。每天连续剥夺大鼠睡眠18小时，并连续1天（SR 1）、3天（SR 3）或5天（SR 5）允许6小时的随意睡眠机会（即，CSR）。在躯体感觉皮层、额叶皮层、海马和基底前脑中测定IL-1β、TNF-α和BDNF mRNA水平。在整个CSR过程中，大鼠脑、肝脏IL-1β和TNF-α的表达均显著增强。相比之下，SR 1天后皮质中BDNF mRNA水平与基线值相似，SR 5天后海马中BDNF mRNA水平显著低于基线值。在基底前脑中，BDNF表达在CSR的5天内保持升高，尽管IL-1β表达显著降低。IL-1β和TNF-α的慢性升高和BDNF的抑制可能导致CSR后报告的SWA反应缺乏。此外，CSR诱导的脑炎症分子的增强和海马BDNF的减弱可能有助于CSR引起的神经认知和警觉性的改善。
Acute sleep loss increases pro-inflammatory and synaptic plasticity-related molecules in the brain, including interleukin-1beta (IL-1β), tumor necrosis factor-alpha (TNF-α), and brain-derived neurotrophic factor (BDNF). These molecules enhance non-rapid eye movement sleep slow wave activity (SWA), also known as electroencephalogram delta power, and modulate neurocognitive performance. Evidence suggests that chronic sleep restriction (CSR), a condition prevalent in today's society, does not elicit the enhanced SWA that is seen after acute sleep loss, although it cumulatively impairs neurocognitive functioning. Rats were continuously sleep deprived for 18 h per day and allowed 6 h of ad libitum sleep opportunity for 1 (SR1), 3 (SR3), or 5 (SR5) successive days (i.e., CSR). IL-1β, TNF-α, and BDNF mRNA levels were determined in the somatosensory cortex, frontal cortex, hippocampus, and basal forebrain. Largely, brain IL-1β and TNF-α expression were significantly enhanced throughout CSR. In contrast, BDNF mRNA levels were similar to baseline values in the cortex after 1 day of SR and significantly lower than baseline values in the hippocampus after 5 days of SR. In the basal forebrain, BDNF expression remained elevated throughout the 5 days of CSR, although IL-1β expression was significantly reduced. The chronic elevations of IL-1β and TNF-α and inhibition of BDNF might contribute to the reported lack of SWA responses reported after CSR. Further, the CSR-induced enhancements in brain inflammatory molecules and attenuations in hippocampal BDNF might contribute to neurocognitive and vigilance detriments that occur from CSR.
登录
查看更多内容
影响因子：
15.1
作者：
Lekander, Mats;Andreasson, Anna Nixon;Axelsson, John
通讯作者：
Axelsson, John
影响因子：
3.4
作者：
Alam, MN;McGinty, D;Szymusiak, R
通讯作者：
Szymusiak, R
影响因子：
9.3
作者：
Song C;Zhang Y;Dong Y
通讯作者：
Dong Y
影响因子：
3.3
作者：
Felger JC;Lotrich FE
通讯作者：
Lotrich FE
影响因子：
15.1
作者：
Yirmiya, Raz;Goshen, Inbal
通讯作者：
Goshen, Inbal