ArticleFrontiers in neuroscience2021
The Suprachiasmatic Nucleus Regulates Anxiety-Like Behavior in Mice.
Article in Frontiers in neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- When the biological clock is disordered: circadian rhythm disruption as a core pathophysiological mechanism in anxiety and depression.Frontiers in psychiatry · 2026Review
- The Key Role of Somatostatin Neurons in the Suprachiasmatic Nucleus in Anxiety-Depression Comorbidity Following Sleep Deprivation.Molecular neurobiology · 2025Article
- Biological Fluid Flows: Signaling Mediums for Circadian Timing.Journal of biological rhythms · 2025Review
- Suprachiasmatic nucleus dysfunction induces anxiety- and depression-like behaviors via activating the BDNF-TrkB pathway of the striatum.Translational psychiatry · 2025Article
- The real-world association between digital markers of circadian disruption and mental health risks.NPJ digital medicine · 2024Article
- Nighttime-specific differential gene expression in suprachiasmatic nucleus and habenula is associated with resilience to chronic social stress.Translational psychiatry · 2024Article
- The sleep-circadian interface: A window into mental disorders.Proceedings of the National Academy of Sciences of the United States of America · 2024Review
- Adolescent circadian rhythm disruption increases reward and risk-taking.Frontiers in neuroscience · 2024Article
- Bidirectional mechanism of comorbidity of depression and insomnia based on synaptic plasticity.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023Article
- CaMKIIa Neurons of the Ventromedial Hypothalamus Mediate Wakefulness and Anxiety-like Behavior.Neurochemical research · 2023Article
- Short-term acute bright light exposure induces a prolonged anxiogenic effect in mice via a retinal ipRGC-CeA circuit.Science advances · 2023Article
- Emotionally clocked out: cell-type specific regulation of mood and anxiety by the circadian clock system in the brain.Frontiers in molecular neuroscience · 2023Review
- Pushing the Frontiers: Optogenetics for Illuminating the Neural Pathophysiology of Bipolar Disorder.International journal of biological sciences · 2023Review
- Time to learn: The role of the molecular circadian clock in learning and memory.Neurobiology of learning and memory · 2022Review
- Altered expression of somatostatin signaling molecules and clock genes in the hippocampus of subjects with substance use disorder.Frontiers in neuroscience · 2022Article
- The Suprachiasmatic Nucleus Regulates Anxiety-Like Behavior in Mice.Frontiers in neuroscience · 2021Article
- Disrupted circadian rhythms and mental health.Handbook of clinical neurology · 2021Review
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Authors and funding
11 authors.
Funding
Abstract
Individuals suffering from mood and anxiety disorders often show significant disturbances in sleep and circadian rhythms. Animal studies indicate that circadian rhythm disruption can cause increased depressive- and anxiety-like behavior, but the underlying mechanisms are unclear. One potential mechanism to explain how circadian rhythms are contributing to mood and anxiety disorders is through dysregulation of the suprachiasmatic nucleus (SCN) of the hypothalamus, known as the "central pacemaker." To investigate the role of the SCN in regulating depressive- and anxiety-like behavior in mice, we chronically manipulated the neural activity of the SCN using two optogenetic stimulation paradigms. As expected, chronic stimulation of the SCN late in the active phase (circadian time 21, CT21) resulted in a shortened period and dampened amplitude of homecage activity rhythms. We also repeatedly stimulated the SCN at unpredictable times during the active phase of mice when SCN firing rates are normally low. This resulted in dampened, fragmented, and unstable homecage activity rhythms. In both chronic SCN optogenetic stimulation paradigms, dampened homecage activity rhythms (decreased amplitude) were directly correlated with increased measures of anxiety-like behavior. In contrast, we only observed a correlation between behavioral despair and homecage activity amplitude in mice stimulated at CT21. Surprisingly, the change in period of homecage activity rhythms was not directly associated with anxiety- or depressive-like behavior. Finally, to determine if anxiety-like behavior is affected during a single SCN stimulation session, we acutely stimulated the SCN in the active phase (zeitgeber time 14-16, ZT14-16) during behavioral testing. Unexpectedly this also resulted in increased anxiety-like behavior. Taken together, these results indicate that SCN-mediated dampening of rhythms is directly correlated with increased anxiety-like behavior. This work is an important step in understanding how specific SCN neural activity disruptions affect depressive- and anxiety-related behavior.
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