Sleep properties of CS mice with spontaneous rhythm splitting in constant darkness

Ebihara, Shizufumi; Miyazaki, Satoru; Sakamaki, Hirotake; Yoshimura, Takashi

doi:10.1016/s0006-8993(03)02947-0

Cited by 8 publications

(2 citation statements)

References 17 publications

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“…CS mice exhibit several distinct phenotypes of circadian behavioral rhythms and sleep properties. For example, CS mice show long free-running periods of over 24 hr (most inbred strains of mice exhibit free-running periods shorter than 24 hrs), spontaneous rhythm splitting and entrainment of circadian rhythms in response to a daily-restricted feeding schedule under constant darkness conditions [5], [6], [7], [8]. In general, abnormal rhythms and sleep patterns are believed to be associated with mental illness.…”

Section: Introductionmentioning

confidence: 99%

Ubiquitin-Specific Peptidase 46 (Usp46) Regulates Mouse Immobile Behavior in the Tail Suspension Test through the GABAergic System

et al. 2012

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The tail suspension test (TST) is widely recognized as a useful experimental paradigm for assessing antidepressant activity and depression-like behavior. We have previously identified ubiquitin-specific peptidase 46 (Usp46) as a quantitative trait gene responsible for decreasing immobility time in the TST in mice. This Usp46 mutation has a 3-bp deletion coding for lysine in the open reading frame, and we indicated that Usp46 is implicated in the regulation of the GABAergic system. However, it is not known precisely how the immobile behavior is regulated by the GABAergic system. Therefore, in the present study, we examined whether the immobility time is influenced by drugs affecting the action mediated by GABAA receptor using both 3-bp deleted (the Usp46 mutant) and null Usp46 (Usp46 KO) mice. Nitrazepam, an agonist at the benzodiazepine-binding site of the GABAA receptor, which potentiates the action of GABA, produced a dose-dependent increase in TST immobility time in the Usp46 mutant mice without affecting general behaviors. The Usp46 KO mice exhibited short immobility times comparable to the Usp46 mutant mice, which was also increased by nitrazepam administration. The effects of nitrazepam in the Usp46 mutant and KO mice were antagonized by flumazenil. These results indicate that the 3-bp deleted Usp46 mutation causes a loss-of-function phenotype, and that the GABAA receptor might participate in the regulation of TST immobility time.

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Section: Introductionmentioning

confidence: 99%

Ubiquitin-Specific Peptidase 46 (Usp46) Regulates Mouse Immobile Behavior in the Tail Suspension Test through the GABAergic System

et al. 2012

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“…The sleep properties are also distinct from those of C57BL/6J (B6) and C3H/He mice, which have normal circadian rhythms. 6 Although B6 and C3H/He mice exhibit clear daily sleep-wake rhythms in the amount of each sleep parameter (awake, SWS (slow-wave sleep), PS (paradoxical sleep)), CS mice do not show clear rhythms in these parameters. The differences are particularly conspicuous in PS.…”

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confidence: 99%

Usp46, encoding a ubiquitin specific peptidase, is a quantitative trait gene underlying “behavioral despair” in mice

Ebihara¹,

Tomida²,

Mamiya

et al. 2010

Sleep and Biological Rhythms

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CS mice exhibit several distinct phenotypes of circadian behavioral rhythms and sleep properties. Because many mental illnesses are associated with abnormalities in the circadian rhythms and sleep pattern, we characterized the behavioral phenotypes in CS mice with a battery of behavioral tests. Among these phenotypes, we found that CS mice exhibit an extremely low immobility time in both the tail suspension test (TST) and forced swimming test (FST). To uncover the genetic basis for lower immobility time, we first performed quantitative trait locus (QTL) mapping using CS and C57BL/6J mice, which revealed significant QTLs on chromosomes (Chrs) 4 (FST) and 5 (TST and FST). To identify the quantitative trait gene on Chr 5, we narrowed the QTL interval to 0.5 Mb using several congenic and subcongenic strains. Ubiquitin-specific peptidase 46 (Usp46) with a lysine codon deletion was located in this region. This deletion affected nest-building, muscimol-induced righting reflex, and anti-immobility effects of imipramine. The muscimol-induced current in the hippocampal CA1 pyramidal neurons and hippocampal expression of the 67-kDa isoform of glutamic acid decarboxylase significantly decreased in Usp46 mutant mice. All these phenotypes were rescued in transgenic mice with bacterial artificial chromosomes containing wild-type Usp46. Thus, Usp46 affects the immobility in the TST and FST, and it is implicated in the regulation of GABA action.The CS mouse is an inbred strain originally established by the hybridization of the NBC and SII strains, which are both now extinct. CS mice exhibit several distinct phenotypes of circadian rhythms and sleep properties. Although in most of the inbred strains of mice, a freerunning circadian period is shorter than 24 h under constant darkness (DD), 1 CS mice have a longer circadian period than 24 h. These unusual circadian rhythms sometime spontaneously split into two activity components and interestingly these rhythms can entrain to a

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Diurnal variation of lipopolysaccharide-induced alterations in sleep and body temperature of interleukin-6-deficient mice

Morrow

Opp

2005

Brain, Behavior, and Immunity

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Sleep properties of CS mice with spontaneous rhythm splitting in constant darkness

Cited by 8 publications

References 17 publications

Ubiquitin-Specific Peptidase 46 (Usp46) Regulates Mouse Immobile Behavior in the Tail Suspension Test through the GABAergic System

Ubiquitin-Specific Peptidase 46 (Usp46) Regulates Mouse Immobile Behavior in the Tail Suspension Test through the GABAergic System

Usp46, encoding a ubiquitin specific peptidase, is a quantitative trait gene underlying “behavioral despair” in mice

Diurnal variation of lipopolysaccharide-induced alterations in sleep and body temperature of interleukin-6-deficient mice

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