Increasing evidence suggests that patients with substance use disorders demonstrate sleep and circadian rhythm disruptions. Not surprisingly, decades of research support changes in brain circuits and neurotransmitter function that also regulate sleep and arousal states. Given that sleep is imperative for memory consolidation and neuronal plasticity, sleep disturbances associated with SUD likely contribute to cognitive impairments- both of which are related to risk of relapse. Thus, understanding drug-induced changes, both short-term and persisting during abstinence as well as understanding underlying sleep/circadian rhythm dysregulation as risk factors that may increase vulnerability to SUD will aid in our ability to better treat or prevent SUDs.
Despite decades of research providing substantial knowledge regarding drug-induced brain changes, understanding how sleep/circadian rhythm disruptions relate to SUD are in their infancy. Pairing multiple neuroscience techniques (EEG, chemo- and opto-genetics approaches) to provide temporal and state-specific manipulations (rapid eye movement sleep, slow-wave sleep) along with novel animal models provide unprecedented potential to understand the role for sleep/circadian disruptions to affect the cycle associated with substance use disorders.
The aim of the current Research Topic is to highlight promising, recent, and novel research examining factors (e.g. genetic, environmental, neurobiological, pharmacological) detailing sleep or circadian rhythm disruptions that contribute to the progression of SUDs or persist during abstinence and may influence recovery or risk of relapse. Areas to be covered in this Research Topic may include, but are not limited to:
- Examination of sleep/wake architecture or circadian rhythms in patients with, or preclinical models of Substance Use Disorders (Opioid, stimulant, EtOH, nicotine, or other).
- Examination of how neuronal, regional, circuit-specific, or global brain function affects sleep/circadian rhythm that influences vulnerability or sensitivity to various drugs.
- Application of neuroscience techniques to probe cell-type specific, ensemble-, or circuit-specific activity implicated in sleep/circadian rhythm disruptions following drug exposure.
- Translational approaches to normalize dysregulations in sleep or circadian rhythms as novel treatment approaches (e.g. pharmacological, environmental, or electrical).