Slow-wave sleep is controlled by a subset of nucleus accumbens core neurons in mice.

Sleep control is ascribed to a two-process model, a widely accepted concept that posits homoeostatic drive and a circadian process as the major sleep-regulating factors. Cognitive and emotional factors also influence sleep-wake behaviour; however, the precise circuit mechanisms underlying their effects on sleep control are unknown. Previous studies suggest that adenosine has a role affecting behavioural arousal in the nucleus accumbens (NAc), a brain area critical for reinforcement and reward.

Adenosine A receptor deficiency attenuates the somnogenic effect of prostaglandin D in mice.

Prostaglandin D (PGD) is one of the most potent endogenous sleep promoting substances. PGD activates the PGD receptor (DPR) and increases the extracellular level of adenosine in wild-type (WT) mice but not DPR knockout (KO) mice, suggesting that PGD-induced sleep is DPR-dependent, and adenosine may be the signaling molecule that mediates the somnogenic effect of PGD. The aim of this study was to determine the involvement of the adenosine A receptor (AR) in PGD-induced sleep.

Interleukin-1β induces sleep independent of prostaglandin D in rats and mice.

Interleukin-1β (IL-1β) and prostaglandin (PG) D are endogenous sleep-promoting substances. Since it was reported that a highly selective cyclooxygenase-2 (COX-2) inhibitor, NS398, completely inhibited IL-1β-induced sleep in rats, IL-1β-induced sleep had been believed to be mediated by prostanoids, most probably PGD. However, in the present study, pretreatment of rats with NS398 (3mg/kg) did not suppress the 64.