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Opioid dependence is defined by an aversive withdrawal syndrome upon drug cessation that can motivate continued drug-taking, development of opioid use disorder, and precipitate relapse. An understudied but common opioid withdrawal symptom is disrupted sleep, reported as both insomnia and daytime sleepiness. Despite the prevalence and severity of sleep disturbances during opioid withdrawal, there is a gap in our understanding of their interactions. The goal of this study was to establish an in-depth, temporal signature of spontaneous oxycodone withdrawal effects on the diurnal composition of discrete sleep stages and the dynamic spectral properties of the electroencephalogram (EEG) signal in male rats. We continuously recorded EEG and electromyography (EMG) signals for 8 d of spontaneous withdrawal after a 14-d escalating-dose oxycodone regimen (0.5–8.0 mg/kg, 2×d; SC). During withdrawal, there was a profound loss (peaking on days 2–3) and gradual return of diurnal structure in sleep, body temperature, and locomotor activity, as well as decreased sleep and wake bout durations dependent on lights on/off. Withdrawal was associated with significant alterations in the slope of the aperiodic 1/f component of the EEG power spectrum, an established biomarker of arousal level. Early in withdrawal, NREM exhibited an acute flattening and return to baseline of both low (1–4 Hz) and high (15–50 Hz) frequency components of the 1/f spectrum. These findings suggest temporally dependent withdrawal effects on sleep, reflecting the complex way in which the allostatic forces of opioid withdrawal impinge upon sleep and diurnal processes. These foundational data based on continuous tracking of vigilance state, sleep stage composition, and spectral EEG properties provide a detailed construct with which to form and test hypotheses on the mechanisms of opioid-sleep interactions.

Sleep remains a major mystery of biology. In particular, little is known about the mechanisms that account for the drive to sleep. In an unbiased screen of more than 12,000 Drosophila lines, we identified a single gene, nemuri, that induces sleep. The NEMURI protein is an antimicrobial peptide that can be secreted ectopically to drive prolonged sleep (with resistance to arousal) and to promote survival after infection. Loss of nemuri increased arousability during daily sleep and attenuated the acute increase in sleep induced by sleep deprivation or bacterial infection. Conditions that increase sleep drive induced expression of nemuri in a small number of fly brain neurons and targeted it to the sleep-promoting, dorsal fan-shaped body. We propose that NEMURI is a bona fide sleep homeostasis factor that is particularly important under conditions of high sleep need; because these conditions include sickness, our findings provide a link between sleep and immune function.

Chronic usage of opioids can result in the development of highly aversive withdrawal symptoms such as dysphoria, increased pain sensitivity and sleep disturbances/insomnia. Experiencing these symptoms during chronic opioid administration is thought to facilitate development of opioid use disorder; a debilitating disorder characterized by escalating, compulsive drug use despite harmful consequences, a constellation of aversive withdrawal signs, cravings, relapse and an increased risk of death. Despite a growing body of research suggesting that opioid withdrawal can disrupt sleep, and produce insomnia or daytime sleepiness, opioid related sleep disturbances have not been rigorously characterized. Therefore, there is a gap in our understanding of how sleep disturbances manifest throughout chronic opioid administration and withdrawal. The goal of this study was to establish an in-depth, temporal characterization of how oxycodone withdrawal affects sleep. Rats were made dependent on the prescription opioid oxycodone via subcutaneously implanted drug pumps that delivered two oxycodone or saline infusions per day (ZT hours 0-2 and 12-14) in escalating doses for 14 days. Upon cessation of oxycodone delivery, somatic withdrawal signs such as ptosis, teeth chattering, head bobs, repetitive sniffing, and flattened posture emerged spontaneously. Electroencephalogram (EEG) and electromyogram signals were wirelessly and continuously recorded for the 14-day oxycodone regimen and for 8 days of spontaneous withdrawal. During withdrawal, there was a profound loss of diurnal rhythms of sleep stages [i.e., rapid eye movement (REM), non-REM (NREM), and Wake], temperature, and locomotor activity that returned to baseline levels after several days. Sleep stage fragmentation also increased. From EEG spectral analysis, I found that the daily rhythmicity of relative NREM power across multiple frequency bands was dampened, and the slope of the NREM EEG power spectrum was flattened suggesting an increase in local non-oscillatory activity. Together, these data provide temporal and mechanistic explanations for the clinical descriptions of “insomnia” and “daytime sleepiness” that are self-reported by opioid-dependent people during withdrawal. Given the large literature on the gradual emergence of aversive withdrawal signs during chronic opioid administration, I performed exploratory analyses of sleep architecture and dynamics data collected during the 14-d escalating-dose oxycodone regimen. The loss of daily sleep rhythmicity and structure observed during withdrawal began to emerge after 3-7 days of oxycodone infusions. In contrast, withdrawal-associated disruptions in EEG spectral properties did not emerge during oxycodone administration. These findings suggest that the allostatic forces of chronic opioids and withdrawal impact sleep through neuroadaptations in diverse neural circuits. In summary, these foundational data provide a detailed construct with which to form and test hypotheses on the mechanisms of opioid-sleep interactions.

Portland's guard Alec Wintering, who was five assists shy of the school record, suffered a season-ending knee injury in Portland's loss on Thursday.

Bilas continued to say the Bulldogs will finish the regular season undefeated and earn a No. 1 seed for the NCAA tournament.

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The Kennel is a major reason the McCarthey Athletic Center remains one of the toughest places to play in college basketball.

Beginning in the early 2000s, it has become common for the faces of players, coaches, celebrities -- and on some occasions President-elect Donald Trump -- to be seen held high above student sections during college basketball games.

LaRae Wiley, executive director at the Salish School of Spokane, sang the national anthem in the Salish language as a tribute to Native American Heritage Month, which was being honored Friday at the McCarthey Athletic Center.

After Grant scored 17 points in the first half, Melson put the clamps down on the BU guard before the Zags finished the half in a zone.