Sleep and immune function: glial contributions and consequences of aging

被引：150

作者：

Ingiosi, Ashley M. ^{[1
,2
]}

Opp, Mark R. ^{[2
,3
]}

Krueger, James M. ^{[4
,5
,6
]}

机构：

[1] Univ Michigan, Grad Program Neurosci, Ann Arbor, MI 48109 USA

[2] Univ Washington, Dept Anesthesiol & Pain Med, Seattle, WA 98195 USA

[3] Univ Washington, Program Neurobiol & Behav, Seattle, WA 98195 USA

[4] Washington State Univ, WWAMI Med Educ Program, Spokane, WA 99202 USA

[5] Washington State Univ, Sleep & Performance Res Ctr, Spokane, WA USA

[6] Washington State Univ, Program Neurosci, Pullman, WA 99164 USA

来源：

CURRENT OPINION IN NEUROBIOLOGY | 2013年 / 23卷 / 05期

基金：

美国国家卫生研究院;

关键词：

SICKNESS BEHAVIOR; P2X(7) RECEPTOR; NEURONAL DAMAGE; AGED MICE; IN-VIVO; EXPRESSION; ADENOSINE; INTERLEUKIN-6; BRAIN; MICROGLIA;

D O I：

10.1016/j.conb.2013.02.003

中图分类号：

Q189 [神经科学];

学科分类号：

071006 [神经生物学];

摘要：

The reciprocal interactions between sleep and immune function are well-studied. Insufficient sleep induces innate immune responses as evidenced by increased expression of pro-inflammatory mediators-in the brain and periphery. Conversely, immune challenges upregulate immunomodulator expression, which alters central nervous system-mediated processes and behaviors, including sleep. Recent studies indicate that glial cells, namely microglia and astrocytes, are active contributors to sleep and immune system interactions. Evidence suggests glial regulation of these interactions is mediated, in part, by adenosine and adenosine 5'-triphosphate actions at purinergic type 1 and type 2 receptors. Furthermore, microglia and astrocytes may modulate declines in sleep wake behavior and immunity observed in aging.

引用

页码：806 / 811

页数：6

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