Schizophrenia bulletinMar 5, 2016

Sleep and Wake Cycle Disruptions in a Mouse Model Lacking a Protein Linked to Schizophrenia

Circadian Biology Weekly Brief ↗PubMed ↗DOI ↗

Updated Apr 1, 2026

Abstract

STOP null mice sleep less overall and exhibit more fragmented sleep patterns compared to wild-type mice.

At baseline, STOP null mice spent more time awake and less time in non-rapid eye movement sleep (NREMS) over a 24-hour period.
STOP null mice showed more frequent transitions between wake and NREMS, particularly during the dark phase.
The distribution of sleep states—wake, NREMS, and REM sleep—differed between STOP null and wild-type mice.
Electroencephalogram (EEG) features also varied by genotype, indicating differences in sleep architecture.
Following sleep deprivation, both STOP null and wild-type mice exhibited increases in overall sleep duration, with similar compensatory sleep intensity.

Simplified

Disruption of sleep/wake cycles is common in patients with schizophrenia and correlates with cognitive and affective abnormalities. Mice deficient in stable tubule only polypeptide (STOP) show cognitive, behavioral, and neurobiological deficits that resemble those seen in patients with schizophrenia, but little is known about their sleep phenotype. We characterized baseline sleep/wake patterns and recovery sleep following sleep deprivation in STOP null mice. Polysomnography was conducted in adult male STOP null and wild-type (WT) mice under a 12:12 hours light:dark cycle before, during, and after 6 hours of sleep deprivation during the light phase. At baseline, STOP null mice spent more time awake and less time in non-rapid eye movement sleep (NREMS) over a 24-hour period, with more frequent transitions between wake and NREMS, compared to WT mice, especially during the dark phase. The distributions of wake, NREMS and REMS across the light and the dark phases differed by genotype, and so did features of the electroencephalogram (EEG). Following sleep deprivation, both genotypes showed homeostatic increases in sleep duration, with no significant genotype differences in the initial compensatory increase in sleep intensity (EEG delta power). These results indicate that STOP null mice sleep less overall, and their sleep and wake periods are more fragmented than those of WT mice. These features in STOP null mice are consistent with the sleep patterns observed in patients with schizophrenia.

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Sleep and Wake Cycle Disruptions in a Mouse Model Lacking a Protein Linked to Schizophrenia

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