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High times for cannabis: Epigenetic imprint and its legacy on brain and behavior

Published

3 years ago

May 17, 2017

Republished by Plato

Review

. 2018 Feb;85:93-101.

doi: 10.1016/j.neubiorev.2017.05.011. Epub 2017 May 12.

Affiliations

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Review

Henrietta Szutorisz et al. Neurosci Biobehav Rev. 2018 Feb.

Free PMC article

. 2018 Feb;85:93-101.

doi: 10.1016/j.neubiorev.2017.05.011. Epub 2017 May 12.

Affiliations

¹ Friedman Brain Institute, Departments of Psychiatry and Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
² Friedman Brain Institute, Departments of Psychiatry and Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Addiction Institute at Mount Sinai, New York, NY, USA. Electronic address: yasmin.hurd@mssm.edu.

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Abstract

Extensive debates continue regarding marijuana (Cannabis spp), the most commonly used illicit substance in many countries worldwide. There has been an exponential increase of cannabis studies over the past two decades but the drug’s long-term effects still lack in-depth scientific data. The epigenome is a critical molecular machinery with the capacity to maintain persistent alterations of gene expression and behaviors induced by cannabinoids that have been observed across the individual’s lifespan and even into the subsequent generation. Though mechanistic investigations regarding the consequences of developmental cannabis exposure remain sparse, human and animal studies have begun to reveal specific epigenetic disruptions in the brain and the periphery. In this article, we focus attention on long-term disturbances in epigenetic regulation in relation to prenatal, adolescent and parental germline cannabinoid exposure. Expanding knowledge about the protracted molecular memory could help to identify novel targets to develop preventive strategies and treatments for behaviors relevant to neuropsychiatric risks associated with developmental cannabis exposure.

Keywords: Adolescence; Cannabinoid; Chromatin; DNA methylation; Epigenetics; Multigenerational inheritance; Prenatal development; Synaptic plasticity; Transcription.

Figures

**Figure 1. Cannabis exposure during sensitive periods of development can impact epigenetic mechanisms, leading to persistent gene regulation and behavioral alterations**

The two most likely populations to use cannabis are pregnant women and adolescents (indicated by green arrow on top). These developmental phases also correspond to periods when the brain is most vulnerable to the influence of external cannabinoids via interfering with epigenetic mechanisms (shown below the schematic of the developmental cycle). Several epigenetic mechanisms that are relevant to the effects of cannabinoids can interfere with normal gene expression via interacting with *DNA* elements (e.g. promoters) and transcription factors (proteins that bind to the DNA) to regulate mRNA transcript levels from a gene. Specific regulatory mechanisms include DNA methylation (Me), positioning and post-translational modifications of nucleosomes (small blue balls), recruitment of the transcription complex (sequence-specific and basal transcription factors, RNA polymerase II), and non-coding RNAs. DNA methyltranserases (DNMT) generate 5-methylcytosine (pink stars) at CpG sites. Ten-eleven translocation (TET) proteins mediate the oxidation of 5-methylcytosine to 5-hydroxymethylcytosine (green stars), leading to demethylation of the DNA. Modifications of nucleosomal histone tails such as methylation (Me) and acetylation (Ac) are mediated by histone methyltransferases (HMT) and histone acetyltransferases (HAT), respectively. Small RNAs are produced from specific genes and either influence the transcription process or target protein-coding messenger RNAs for degradation. Germ cells (sperm, oocyte) are also sensitive to cannabinoids but the exact underlying epigenetic mechanisms remain to be determined.

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[Neurodevelopment and Cannabis].

Krebs MO, Demars F, Frajerman A, Kebir O, Jay T. Krebs MO, et al. Bull Acad Natl Med. 2020 Apr 17;204(6):561-9. doi: 10.1016/j.banm.2020.04.002. Online ahead of print. Bull Acad Natl Med. 2020. PMID: 32308209 Free PMC article. Review. French.
Cannabis use and the sperm epigenome: a budding concern?

Schrott R, Murphy SK. Schrott R, et al. Environ Epigenet. 2020 Mar 19;6(1):dvaa002. doi: 10.1093/eep/dvaa002. eCollection 2020 Jan. Environ Epigenet. 2020. PMID: 32211199 Free PMC article. Review.
Harmful Effects of Smoking Cannabis: A Cerebrovascular and Neurological Perspective.

Archie SR, Cucullo L. Archie SR, et al. Front Pharmacol. 2019 Dec 6;10:1481. doi: 10.3389/fphar.2019.01481. eCollection 2019. Front Pharmacol. 2019. PMID: 31920665 Free PMC article. Review.
Gestational exposure to the cannabinoid WIN 55,212-2 and its effect on the innate intestinal immune response.

Hernández-Cervantes R, Pérez-Torres A, Prospéro-García Ó, Morales Montor J. Hernández-Cervantes R, et al. Sci Rep. 2019 Dec 30;9(1):20340. doi: 10.1038/s41598-019-56653-y. Sci Rep. 2019. PMID: 31889093 Free PMC article.

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Source: https://pubmed.ncbi.nlm.nih.gov/28506926/?utm_source=no_user_agent&utm_medium=rss&utm_campaign=pubmed-2&utm_content=1z7zlNEMzQex5jriqkhCblNtckSEpT9xYlxxeymU_73UTETESY&fc=20200804213258&ff=20200810171721&v=2.11.5

Related Topics:cannabinoid cannabis COVID-19 Data development heartland marijuana medicine regulation Regulatory research search

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