Journal
BIOMEDICINE & PHARMACOTHERAPY
Volume 153, Issue -, Pages -Publisher
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2022.113333
Keywords
Circadianrhythms; Bmal1; Cocaine; GluA1; GluA2
Funding
- Ministerio de Ciencia e Innovacion
- Ministerio de Sanidad (Retic-ISCIII) [PID2019-104077RB-100]
- FPI from the Ministerio de Economia y Competividad [RD16/017/010, RD21/0009/0001, 2018/007]
- MCIN/AEI [BES-2017- 080066, PRE2020-091923]
- ESF Investing in your future [PID2019-104077RB-100]
- AEI
- ICREA Academia Award (Institucio Catalana de Recerca i Estudis Avanats, Generalitat de Catalunya) [RD16/017/010]
- [RYC2019-026661-I]
- [CEX2018-000792-M]
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The study found that mice with Bmal1 gene deletion exhibited behavioral and neurobiological changes, including decreased adaptability to the environment and social recognition impairments. Additionally, these mice showed reduced rewarding effects of cocaine and decreased cocaine-seeking behavior.
Brain and Muscle Arnt-like Protein 1 (BMAL1) is an essential component of the molecular clock underlying circadian rhythmicity. Its function has been recently associated with mood and reward processing alterations. We investigated the behavioural and neurobiological impact of Bmal1 gene deletion in mice, and how this could affect rewarding effects of cocaine. Additionally, key clock genes and components of the dopamine system were assessed in several brain areas. Our results evidence behavioural alterations in Bmal1-KO mice, including changes in locomotor activity with impaired habituation to environments, short-term memory and social recognition impairments. In addition, Bmal1-KO mice experienced reduced cocaine-induced sensitisation and rewarding effects of cocaine as well as reduced cocaine-seeking behaviour. Furthermore, Bmal1 deletion influenced the expression of other clock-related genes in the mPFC and striatum, as well as alterations in the expression of dopaminergic elements. Overall, the present article offers a novel and extensive characterisation of Bmal1-KO animals. We suggest that reduced cocaine's rewarding effects in these mutant mice might be related to Bmal1 role as an expression regulator of MAO and TH, two essential enzymes involved in dopamine metabolism.
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