ArticleBiological psychiatry2018
Circadian Disruptions in the Myshkin Mouse Model of Mania Are Independent of Deficits in Suprachiasmatic Molecular Clock Function.
Article in Biological psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Circadian Influences on the Habenula and Their Potential Contribution to Neuropsychiatric Disorders.Frontiers in behavioral neuroscience · 2021Pooled it
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- Autistic behavior is a common outcome of biallelic disruption of PDZD8 in humans and mice.Molecular autism · 2025Article
- Loss of neuropeptide signalling alters temporal expression of mouse suprachiasmatic neuronal state and excitability.The European journal of neuroscience · 2024Article
- The Oxidative Status and NaBioMed research international · 2024Article
- A novel murine model of mania.Molecular psychiatry · 2023Article
- NaBiomedicines · 2023Review
- Blue Light Blocking Treatment for the Treatment of Bipolar Disorder: Directions for Research and Practice.Journal of clinical medicine · 2022Review
- Article
- Genetically altered animal models for ATP1A3-related disorders.Disease models & mechanisms · 2021Article
- Dysfunction of ventral tegmental area GABA neurons causes mania-like behavior.Molecular psychiatry · 2021Article
- Article
- Keeping time in the lamina terminalis: Novel oscillator properties of forebrain sensory circumventricular organs.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Na⁺, K⁺-ATPase Signaling and Bipolar Disorder.International journal of molecular sciences · 2018Review
- Circadian Rhythm Disturbances in Mood Disorders: Insights into the Role of the Suprachiasmatic Nucleus.Neural plasticity · 2017Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
backgroundAlterations in environmental light and intrinsic circadian function have strong associations with mood disorders. The neural origins underpinning these changes remain unclear, although genetic deficits in the molecular clock regularly render mice with altered mood-associated phenotypes.
methodsA detailed circadian and light-associated behavioral characterization of the Na
resultsIn vivo assays revealed several circadian abnormalities including lengthened period and instability of behavioral rhythms, and elevated metabolic rate. Grossly aberrant responses to light included accentuated resetting, accelerated re-entrainment, and an absence of locomotor suppression. Bioluminescent recording of circadian clock protein (PERIOD2) output from ex vivo SCN revealed no deficits in Myk/+ molecular clock function. Optic nerve crush rescued the circadian period of Myk/+ behavior, highlighting that afferent inputs are critical upstream mediators. Electrophysiological and calcium imaging SCN recordings demonstrated changes in the response to glutamatergic stimulation as well as the electrical output indicative of altered retinal input processing.
conclusionsThe Myshkin model demonstrates profound circadian and light-responsive behavioral alterations independent of molecular clock disruption. Afferent light signaling drives behavioral changes and raises new mechanistic implications for circadian disruption in affective disorders.
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