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Trajectory of adolescent cannabis use on addiction vulnerability

The adolescent brain is a period of dynamic development making it vulnerable to environmental factors such as drug exposure. Of the illicit drugs, cannabis is most used by teenagers since it is perceived by many to be of little harm. This perception has led to a growing number of states approving its legalization and increased accessibility. Most of the debates and ensuing policies regarding cannabis were done without consideration of its impact on one of the most vulnerable population, namely…

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. 2014 Jan;76 Pt B(0 0):416-24.

doi: 10.1016/j.neuropharm.2013.07.028. Epub 2013 Aug 14.

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Yasmin L Hurd et al. Neuropharmacology. .

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Abstract

The adolescent brain is a period of dynamic development making it vulnerable to environmental factors such as drug exposure. Of the illicit drugs, cannabis is most used by teenagers since it is perceived by many to be of little harm. This perception has led to a growing number of states approving its legalization and increased accessibility. Most of the debates and ensuing policies regarding cannabis were done without consideration of its impact on one of the most vulnerable population, namely teens, or without consideration of scientific data. We provide an overview of the endocannabinoid system in relation to adolescent cannabis exposure and provide insights regarding factors such as genetics and behavioral traits that confer risk for subsequent addiction. While it is clear that more systematic scientific studies are needed to understand the long-term impact of adolescent cannabis exposure on brain and behavior, the current evidence suggests that it has a far-reaching influence on adult addictive behaviors particularly for certain subsets of vulnerable individuals. This article is part of a Special Issue entitled ‘NIDA 40th Anniversary Issue’.

Keywords: Cannabinoid; Marijuana; Nucleus accumbens; Opioid neuropeptide; Prefrontal cortex.

Figures

Figure 1

Figure 1

Cannabinoid receptor mRNA (CNR1) expression in the human brain emphasizes this gene’s abundant expression in cerebral cortex – such as insular cortex (I) and prefrontal cortex (PFC) – as well as the caudate nucleus (CN), putamen (Pu), nucleus accumbens (NAc), hippocampus (Hipp), amygdala (Amy), and cerebellum (CB). Absent-to-low mRNA expression is notable in the thalamus (T), basal forebrain (BF), globus pallidus (GP), and midbrain (Ms).

Figure 2

Figure 2

Schematic illustration of the striatonigral ‘Go’ andstriatopallidal ‘NoGo’ pathways. These medium spiny output neurons are distinguishable based on their targets and subcellular markers, namely the expression of D1R (purple) and D2R (brown), respectively. Both cell-types, however, express CB1R (orange). This dissociation is based mainly on the dorsal striatal circuit, but a similar organization, particularly with respect to the ‘NoGo’ pathway, exists for the ventral striatal circuit.

Figure 3

Figure 3

Periodic low-to-moderate THC exposure during adolescence (1.5 mg/kg every third day between postnatal days 28 and 49) alters Drd2 and Penk mRNA expression in the adult nucleus accumbens. These genes are strongly enriched in striatopallidal neurons of the nucleus accumbens (*p < 0.05).

Figure 4

Figure 4

PENK SNPs (rs2609997 and rs2576573) are associated with PENK expression in the human brain. High-risk alleles for cannabis dependence of the rs2609997 and rs2576573 PENK SNPs associate with elevated mRNA expression and met-enkephalin peptide (met-enk) levels in the human striatum (A). Similarly, these alleles associate with elevated mRNA expression in central amygdala nucleus (B). (High-risk genotypes = C/C + C/T for rs2609997 or A/A + A/G for rs2576573; low-risk genotypes = T/T for rs2609997 or G/G for rs2576573. *p < 0.05.)

Figure 5

Figure 5

Synergistic Contribution of negative affect trait and PENK variants to cannabis dependence vulnerability. (High-risk genotype = C/C + C/T for rs2609997 or A/A + A/G for rs2576573; low-risk genotype = T/T for rs2609997 or G/G for rs2576573. ***p < 0.01; ****p < 0.001. Modified from Jutras-Aswad et al., 2012.)

Figure 6

Figure 6

Schematic overview of the interaction between environmental factors, genetics and behavioral traits that together contribute to complex neuropsychiatric disorders like addiction. Vulnerability involves a delicate balance between factors that promote and protect against disease, and adolescent THC, an environmental factor, may tip this balance in teens with high-risk genotypes and behavioral traits.

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Source: https://pubmed.ncbi.nlm.nih.gov/23954491/?utm_source=no_user_agent&utm_medium=rss&utm_campaign=pubmed-2&utm_content=1z7zlNEMzQex5jriqkhCblNtckSEpT9xYlxxeymU_73UTETESY&fc=20200804213258&ff=20200811164741&v=2.11.5

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