Sleep and immunomodulatory responses to systemic lipopolysaccharide in mice selectively expressing interleukin-1 receptor 1 on neurons or astrocytes
Abstract
Sleep-wake behavior is altered in response to immune challenge. Although the precise mechanisms that govern sickness-induced changes in sleep are not fully understood, interleukin-1β (IL-1) is one mediator of these responses. To better understand mechanisms underlying sleep and inflammatory responses to immune challenge, we used two transgenic mouse strains that express IL-1 receptor 1 (IL1R1) only in the central nervous system and selectively on neurons or astrocytes. Electroencephalographic recordings from transgenic and wild-type mice reveal that systemic challenge with lipopolysaccharide (LPS) fragments sleep, suppresses rapid eye movement sleep (REMS), increases non-REMS (NREMS), diminishes NREM delta power, and induces fever in all genotypes. However, the magnitude of REMS suppression is greater in mice expressing IL1R1 on astrocytes compared with mice in which IL1R1 is selectively expressed on neurons. Furthermore, there is a delayed increase in NREM delta power when IL1R1 is expressed on astrocytes. LPS-induced sleep fragmentation is reduced in mice expressing IL1R1 on neurons. Although LPS increases IL-1 and IL-6 in brain of all genotypes, this response is attenuated when IL1R1 is expressed selectively on neurons or on...Continue Reading
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