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Deconstructing Neuronal and Astroglial Contributions to Sleep and Inflammatory Immune Responses.

Interactions between sleep and immune function are bidirectional. Interleukin-1β (IL-1) is a pro-inflammatory cytokine that regulates sleep. However, the cellular substrates that mediate IL-1 regulation of sleep and immune interactions are not fully elucidated. To this end, we engineered two transgenic mouse lines that express interleukin-1 receptor 1 (IL1R1) only in the central nervous system and selectively on neurons or astrocytes via transcriptional control of the neuron-specific enolase (NSE) or human glial fibrillary acidic protein (gfa2) promoters, respectively. Animals with selective neuronal IL1R1 expression are referred to as NSE-IL1R1, and mice expressing IL1R1 on astrocytes are called GFAP-IL1R1. Spontaneous sleep and temperature phenotypes were determined in transgenic and wild type (WT) mice via electroencephalographic recordings and brain temperature measurements. Under baseline conditions, NSE-IL1R1 and GFAP-IL1R1 mice spend a comparable amount of time in non-rapid eye movement sleep (NREMS) but exhibit more rapid eye movement sleep (REMS) compared to WT. Transgenic mice also have reduced theta power in REMS, enhanced NREM delta power, and lower brain temperatures compared to WT mice. In response to 6 h of sleep deprivation,