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Cannabidiol attenuates cognitive deficits and neuroinflammation induced by early alcohol exposure in a mice model

View ORCID ProfileAlba García-Baos, View ORCID ProfileXavi Puig-Reyne, View ORCID ProfileÓscar García-Algar, View ORCID ProfileOlga Valverde
doi: https://doi.org/10.1101/2021.03.16.435465
Alba García-Baos
1Neurobiology of Behaviour Research Group (GReNeC-NeuroBio), Department of Experimental and Health Sciences, Universitat Pompeu Fabra, Barcelona, Spain
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Xavi Puig-Reyne
1Neurobiology of Behaviour Research Group (GReNeC-NeuroBio), Department of Experimental and Health Sciences, Universitat Pompeu Fabra, Barcelona, Spain
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Óscar García-Algar
3Neonatology Unit, ICGON, IDIBAPS, Hospital Clínic-Maternitat, BCNatal, Barcelona, Spain
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Olga Valverde
1Neurobiology of Behaviour Research Group (GReNeC-NeuroBio), Department of Experimental and Health Sciences, Universitat Pompeu Fabra, Barcelona, Spain
2Neuroscience Research Programme, IMIM-Hospital del Mar Research Institute, Barcelona, Spain
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  • For correspondence: olga.valverde@upf.edu
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Summary

Foetal alcohol spectrum disorder (FASD) is the umbrella term used to describe the physical and mental disabilities induced by alcohol exposure during development. Early alcohol exposure induces cognitive impairments resulting from damage to the central nervous system (CNS). The neuroinflammatory response accompanied by neurodegenerative mechanisms contribute to those detrimental alterations. Cannabidiol (CBD) has recently emerged as an anti-inflammatory drug that might be useful to treat several neuropsychiatric disorders. In our study, we assessed the effects of CBD on long-lasting cognitive deficits induced by early alcohol exposure. Furthermore, we analysed long-term pro-inflammatory and apoptotic markers within the prefrontal cortex and hippocampus. To model alcohol binge drinking during gestational and lactation periods, we used pregnant C57BL/6 female mice with time-limited access to 20% v/v alcohol solution. Following the prenatal and lactation alcohol exposure (PLAE), we treated the male and female offspring with CBD from post-natal day (PD) 25 until PD34, and we evaluated their cognitive performance at PD60. Our results showed that CBD treatment during peri-adolescence period ameliorates cognitive deficits observed in our FASD-like mouse model, without sex differences. Moreover, CBD restores the PLAE-induced increased levels of TNFα and IL-6 in the hippocampus. Thus, our study provides new insights for CBD as a therapeutic agent to counteract cognitive impairments and neuroinflammation caused by early alcohol exposure.

Competing Interest Statement

The authors have declared no competing interest.

  • ABBREVIATIONS

    CBD
    cannabidiol
    CNS
    central nervous system
    COX
    cyclooxygenase
    CB1R
    cannabinoid receptor type 1
    CB2R
    cannabinoid receptor type 2
    DID
    drinking in the dark
    FAAH
    fatty acid amide hydrolase enzyme
    FASD
    Foetal alcohol spectrum disorder
    HPC
    hippocampus
    IL
    interleukin
    NF-kB
    nuclear factor Kappa-B
    NLRP
    NOD-like receptor protein
    NOL
    novel object location
    NOR
    novel object recognition
    PD
    post-natal day
    PFC
    prefrontal cortex
    PLAE
    prenatal and lactation alcohol exposure
    PPAR
    peroxisome proliferator-activated receptor
    TNFα
    tumor necrosis factor alpha
    TLR4
    toll-like receptor 4
    VEH
    vehicle.
  • Copyright 
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    Posted March 17, 2021.
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    Cannabidiol attenuates cognitive deficits and neuroinflammation induced by early alcohol exposure in a mice model
    Alba García-Baos, Xavi Puig-Reyne, Óscar García-Algar, Olga Valverde
    bioRxiv 2021.03.16.435465; doi: https://doi.org/10.1101/2021.03.16.435465
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    Cannabidiol attenuates cognitive deficits and neuroinflammation induced by early alcohol exposure in a mice model
    Alba García-Baos, Xavi Puig-Reyne, Óscar García-Algar, Olga Valverde
    bioRxiv 2021.03.16.435465; doi: https://doi.org/10.1101/2021.03.16.435465

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