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Cannabidiol modulates the expression of neuroinflammatory factors in stress- and drug-induced reinstatement of methamphetamine in extinguished rats

Methamphetamine (METH) is a highly potent and addictive psychostimulant that is frequently abused worldwide. Although the biggest challenge to the efficient treatment of drug dependence is relapse, its mechanism is completely unclear. Plenty of evidence suggests that inflammation contributes to drug-induced reward especially in brain regions that are involved in the reward system, but there is no document about relapse. Cannabidiol (CBD) is a nonpsychoactive cannabinoid that has powerful…

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. 2020 Mar;25(2):e12740.

doi: 10.1111/adb.12740. Epub 2019 Feb 22.

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Saeideh Karimi-Haghighi et al. Addict Biol. .

Abstract

Methamphetamine (METH) is a highly potent and addictive psychostimulant that is frequently abused worldwide. Although the biggest challenge to the efficient treatment of drug dependence is relapse, its mechanism is completely unclear. Plenty of evidence suggests that inflammation contributes to drug-induced reward especially in brain regions that are involved in the reward system, but there is no document about relapse. Cannabidiol (CBD) is a nonpsychoactive cannabinoid that has powerful anti-inflammatory and immunosuppressive properties. A previous research in our laboratory has demonstrated that CBD prevents reinstatement of METH even in 24-hour rapid eye movement (REM) sleep-deprived (RSD) rats. The aim of this study was to assess whether CBD prevents reinstatement of METH through change of gene expression of cytokines such as interleukin-1β, interleukin-6, interleukin-10, and tumor necrosis factor α (TNF-α) in extinguished rats. Real-time polymerase chain reaction (PCR) was used in this research to assay gene expression of cytokines. We found that stress- and drug-induced reinstatement of METH enhanced mRNA expression of cytokines in the prefrontal cortex (PFC) and hippocampus. Furthermore, CBD treatment significantly reduced the mRNA expression of cytokines in the PFC and hippocampus, but CBD treatment in RSD rats increased expression of cytokines in the hippocampus. It seems that enhancement of cytokines leads to change in neurotransmission and so triggers reinstatement of METH.

Keywords: REM sleep deprivation; cannabidiol; inflammatory cytokines expression; methamphetamine; reinstatement; reward system.

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REFERENCES

    1. Downey LA, Loftis JM. Altered energy production, lowered antioxidant potential, and inflammatory processes mediate CNS damage associated with abuse of the psychostimulants MDMA and methamphetamine. Eur J Pharmacol. 2014;727:125-129.
    1. Mariani JJ, Levin FR. Psychostimulant treatment of cocaine dependence. Psychiatr Clin North Am. 2012;35(2):425-439.
    1. Le Foll B. What does addiction medicine expect from neuroscience? From genes and neurons to treatment responses. Prog Brain Res. 2016;224:419-447.
    1. Mantsch JR, Baker DA, Funk D, Le AD, Shaham Y. Stress-induced reinstatement of drug seeking: 20 years of progress. Neuropsychopharmacology: Off Publ Am Coll Neuropsychopharmacology. 2016;41(1):335-356.
    1. Karimi-Haghighi S, Haghparast A. Cannabidiol inhibits priming-induced reinstatement of methamphetamine in REM sleep deprived rats. Prog Neuropsychopharmacol Biol Psychiatry. 2018;82:307-313.

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Source: https://pubmed.ncbi.nlm.nih.gov/30793820/?utm_source=no_user_agent&utm_medium=rss&utm_campaign=pubmed-2&utm_content=1TQbL92JdzYTve0m3OsSoggMby2JyZDVBLRHiDMYZkT1hs6YNQ&fc=20200804223051&ff=20200816094834&v=2.11.5

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