Author: Thomas Kilduff

We describe here a model of opioid withdrawal in mice that resembles the sleep phenotype characteristic of withdrawal in humans.

Over 40 years have elapsed since the original description of the effects of sodium gamma-hydroxybutyrate (GHB) on sleep [1] and the subsequent description of GHB as an effective treatment for narcolepsy [2, 3], yet the neurobiological basis for its efficacy in narcolepsy remains a mystery.

In the present study, we systematically evaluated the efficacy of two NOPR agonists, Ro64-6198 and SR16835, on sleep/wake in rats, mice, and Cynomolgus macaques.

We evaluated the efficacy of two small molecule hypocretin/orexin receptor-2 (HCRTR2) agonists in narcoleptic male orexin/tTA; TetO-DTA mice.

We compared the development of narcoleptic symptomatology in male vs. female orexin-tTA; TetO-DTA mice, a model in which Hcrt neuron degeneration can be initiated by removal of doxycycline (DOX) from the diet.

Whether the cause of daytime sleepiness in narcolepsy type 1 (NT1) is a direct consequence of the loss of orexin (ORX) neurons or whether low orexin reduces the efficacy of the monoaminergic systems to promote wakefulness is unclear.

Animal models have advanced not only our understanding of the etiology and phenotype of the sleep disorder narcolepsy but have also informed sleep/wake regulation more generally.

The involvement of this system in a disorder characterized by the loss of control over arousal state boundaries also suggested its role as a critical component of endogenous sleep-wake regulatory circuitry.

This study aimed to determine whether ALM produces less acute cognitive impairment than ZOL in human subjects.

Here, we discuss shallow MD as a feasible first step toward synthetic torpor during spaceflight and summarize perspectives following a recent NASA-hosted workshop.