ArticleFrontiers in pharmacology2024
Bmal1 haploinsufficiency impairs fear memory and modulates neuroinflammation via the 5-HT2C receptor.
Article in Frontiers in pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- BMAL1 Overexpression in the SCN Confers Protection Against Anxiety-Like Behaviors of Chronic Sleep Restricted-Mice.Molecular neurobiology · 2026Article
- Microglia-mediated synaptic pruning in neural circuit remodeling: multidimensional control in homeostasis and neuropathology.BMC medicine · 2026Review
- Beyond neurotransmission: the roles of serotonylation in physiological and pathological processes.Cellular & molecular biology letters · 2026Review
- Toward autonomous artificial intelligence agents in sports science: a modular framework for development, validation, and implementation.Biology of sport · 2026Review
- Core Circadian Protein BMAL1: Implication for Nervous System Functioning and Its Diseases.Brain sciences · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
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Abstract
Background: BMAL1, a key regulator of circadian rhythms, plays a multifaceted role in brain function. However, the complex interplay between BMAL1, memory, neuroinflammation, and neurotransmitter regulation remains poorly understood. To investigate these interactions, we conducted a study using BMAL1-haplodeficient mice (BMAL1 Methods: We exposed BMAL1 Results: We found that BMAL1 haploinsufficiency led to deficits in cued fear learning and memory, while spatial memory and object recognition remained intact. Further analysis revealed dysregulated neurotransmitter levels and alterations in neurotransmitter-related proteins in the prefrontal cortex of BMAL1 Conclusion: These findings highlight that BMAL1 haploinsufficiency leads to deficits in fear learning and memory, which are linked to alterations in neurotransmitters and receptors, particularly the 5-HT2C receptor. Targeting the 5-HT2C receptor may offer a potential therapeutic strategy for mitigating cognitive impairments associated with BMAL1 dysfunction.
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Registered trials
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