Total Sleep Deprivation Decreases Immobility In The Forced-Swim Test

Rodríguez, Fernando López; Kim, Joseph; Poland, Russell E.

doi:10.1038/sj.npp.1300406

Cited by 42 publications

(26 citation statements)

References 33 publications

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“…When compared with control mice, we observed a decrease in immobility to both SD- and KT-treated mice ( p < .05, t test) (Figure 1B, left) with no significant difference between treated groups. Our results are consistent with those of other studies (30,37–39). Interestingly, analyzing the activity in 1-minute bins, we observed that all animal groups gradually become immobile, with the saline group being the most immobile.…”

Section: Resultssupporting

confidence: 94%

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A Circadian Genomic Signature Common to Ketamine and Sleep Deprivation in the Anterior Cingulate Cortex

Orozco-Solís

Montellier

Aguilar-Arnal

et al. 2017

Biological Psychiatry

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BACKGROUND Conventional antidepressants usually require several weeks to achieve a full clinical response in patients with major depressive disorder, an illness associated with dysregulated circadian rhythms and a high incidence of suicidality. Two rapid-acting antidepressant strategies, low-dose ketamine (KT) and sleep deprivation (SD) therapies, dramatically reduce depressive symptoms within 24 hours in a subset of major depressive disorder patients. However, it is unknown whether they exert their actions through shared regulatory mechanisms. To address this question, we performed comparative transcriptomics analyses to identify candidate genes and relevant pathways common to KT and SD. METHODS We used the forced swim test, a standardized behavioral approach to measure antidepressant-like activity of KT and SD. We investigated gene expression changes using high-density microarrays and pathway analyses (Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, Gene Set Enrichment Analysis) in KT- and SD-treated mice compared with saline-treated control male mice. RESULTS We show that KT and SD elicit common transcriptional responses implicating distinct elements of the circadian clock and processes involved in neuronal plasticity. There is an overlap of 64 genes whose expression is common in KT and SD. Specifically, there is downregulation of clock genes including Ciart, Per2, Npas4, Dbp, and Rorb in both KT- and SD-treated mice. CONCLUSIONS We demonstrate a potential involvement of the circadian clock in rapid antidepressant responses. These findings could open new research avenues to help design chronopharmacological strategies to treat major depressive disorder.

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Section: Resultssupporting

confidence: 94%

“…Our results showed similar efficacy for SD and KT groups that was significantly different from the saline-treated control group. Antidepressant-like activity on the FST for KT (39,52,53) and SD (30,37) has been previously reported.…”

Section: Discussionmentioning

confidence: 82%

A Circadian Genomic Signature Common to Ketamine and Sleep Deprivation in the Anterior Cingulate Cortex

Orozco-Solís

Montellier

Aguilar-Arnal

et al. 2017

Biological Psychiatry

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“…One night of TSD in rats decreases immobility in the forced swim test, similar to the actions of antidepressant drugs (Lopez-Rodriguez et al, 2004). Furthermore, like antidepressant treatment, TSD in rats stimulates hippocampal neurogenesis (Grassi Zucconi et al, 2006).…”

Section: Treating Mood Disorders By Altering the Circadian Cycle 41 mentioning

confidence: 89%

Circadian genes, rhythms and the biology of mood disorders

McClung

2007

Pharmacology & Therapeutics

585

386

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For many years, researchers have suggested that abnormalities in circadian rhythms may underlie the development of mood disorders such as bipolar disorder, major depression and seasonal affective disorder. Furthermore, some of the treatments that are currently employed to treat mood disorders are thought to act by shifting or "resetting" the circadian clock, including total sleep deprivation and bright light therapy. There is also reason to suspect that many of the mood stabilizers and antidepressants used to treat these disorders may derive at least some of their therapeutic efficacy by affecting the circadian clock. Recent genetic, molecular and behavioral studies implicate individual genes that make up the clock in mood regulation. As well, important functions of these genes in brain regions and neurotransmitter systems associated with mood regulation is becoming apparent. In this review, the evidence linking circadian rhythms and mood disorders, and what is known about the underlying biology of this association, is presented.

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“…On the other hand, TSD could increase serotonin concentrations in different areas of the brain including hippocampus (45). Behavioral tests have also shown the antidepressant effects of TSD in animal models (46). The antidepressant effect of SD is, however, not believed to be related to the associated anxiolytic-like process (47).…”

Section: Discussionmentioning

confidence: 99%

Aversive Memory, Anxiety-Related Behaviors, and Serum Neurochemical Levels in a Rat Model of Labored Sleep Loss

et al. 2014

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Background: Sleep deprivation (SD) is emerging as a hot topic due to its health concerns. There are compelling reasons for a tremendous interest in neuroscience of sleep in recent years. Objectives: We aimed to evaluate how total sleep deprivation (TSD) and chronic partial sleep restriction (CPSR) might affect memory, anxiety-related behaviors, and the serum level of neurochemical markers such as brain-derived neurotrophic factor (BDNF) and corticosterone in a rat model. Materials and Methods:The disk-over-water (DOW) apparatus was employed to induce TSD and CPSR in male Wistar rats. The six study arms were as follows: cage control, 48 hours; cage control, seven days; DOW control, 48 hours; DOW control, seven days, TSD, and CPSR. Elevated plus-maze (EPM) was used to measure parameters (percentage of OAT, percentage of OAE, and locomotor activity) corresponding to anxiety and aversive memory. To measure serum BDNF and corticosterone levels using the ELISA method, blood samples were drawn from all rats on the fourth day at 5 P.M. Results: Our results demonstrated that TSD (P < 0.001) and CPSR (P < 0.001) induce memory impairment while exert anxiolytic-like effects in comparison with controls. Data showed that CPSR causes more memory impairment and anxiolytic-like effect in comparison to TSD (P < 0.001).These interventions however, did not alter the locomotor activity. Serum corticosterone level raised dramatically in CPSR rats in comparison to TSD and controls. Although the difference in serum BDNF level between TSD and CPSR arms was insignificant, it was markedly decreased in comparison to corresponding controls (P < 0.001). Conclusions: Our findings suggest the more pronounced effect of CPSR rather than TSD in impairing aversive memory and reducing anxiety. Decreased BDNF and peaked corticosterone level in TSD and CPSR suggest the probable inflammatory processes involved in possible insults to the brain caused by SD.

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Total Sleep Deprivation Decreases Immobility In The Forced-Swim Test

Cited by 42 publications

References 33 publications

A Circadian Genomic Signature Common to Ketamine and Sleep Deprivation in the Anterior Cingulate Cortex

A Circadian Genomic Signature Common to Ketamine and Sleep Deprivation in the Anterior Cingulate Cortex

Circadian genes, rhythms and the biology of mood disorders

Aversive Memory, Anxiety-Related Behaviors, and Serum Neurochemical Levels in a Rat Model of Labored Sleep Loss

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