Limits...
Long-term consequences of adolescent cannabinoid exposure in adult psychopathology.

Renard J, Krebs MO, Le Pen G, Jay TM - Front Neurosci (2014)

Bottom Line: The endocannabinoid system plays an important role in development by acting on synaptic plasticity, neuronal cell proliferation, migration, and differentiation.Thus, over-activation of the endocannabinoid system by chronic exposure to CB1R agonists (e.g., THC, CP-55,940, and WIN55,212-2) during adolescence can dramatically alter brain maturation and cause long-lasting neurobiological changes that ultimately affect the function and behavior of the adult brain.Here, we review the relationship between cannabinoid exposure during adolescence and the increased risk of neuropsychiatric disorders, focusing on both clinical and animal studies.

View Article: PubMed Central - PubMed

Affiliation: Laboratoire de Physiopathologie des maladies Psychiatriques, UMR_S894 Institut National de la Santé et de la Recherche Médicale, Centre de Psychiatrie et Neurosciences Paris, France ; Centre Hospitalier Sainte-Anne, Service Hospitalo Universitaire, Faculté de Médecine Paris Descartes, Université Paris Descartes Paris, France.

ABSTRACT
Marijuana is the most widely used illicit drug among adolescents and young adults. Unique cognitive, emotional, and social changes occur during this critical period of development from childhood into adulthood. The adolescent brain is in a state of transition and differs from the adult brain with respect to both anatomy (e.g., neuronal connections and morphology) and neurochemistry (e.g., dopamine, GABA, and glutamate). These changes are thought to support the emergence of adult cerebral processes and behaviors. The endocannabinoid system plays an important role in development by acting on synaptic plasticity, neuronal cell proliferation, migration, and differentiation. Delta-9-tetrahydrocanabinol (THC), the principal psychoactive component in marijuana, acts as a partial agonist of the cannabinoid type 1 receptor (CB1R). Thus, over-activation of the endocannabinoid system by chronic exposure to CB1R agonists (e.g., THC, CP-55,940, and WIN55,212-2) during adolescence can dramatically alter brain maturation and cause long-lasting neurobiological changes that ultimately affect the function and behavior of the adult brain. Indeed, emerging evidence from both human and animal studies demonstrates that early-onset marijuana use has long-lasting consequences on cognition; moreover, in humans, this use is associated with a two-fold increase in the risk of developing a psychotic disorder. Here, we review the relationship between cannabinoid exposure during adolescence and the increased risk of neuropsychiatric disorders, focusing on both clinical and animal studies.

No MeSH data available.


Related in: MedlinePlus

Schematic overview of the various stages of adolescence in rats. To model the effects of cannabinoid exposure at different developmental stages, rats can be treated chronically throughout the entire adolescent period (from PND28 through PND61) or during specific stages of adolescence, including early adolescence (beginning at PND28), mid-adolescence (beginning at PND38), or late adolescence (beginning at PND49). The long-term effects of adolescent cannabinoid exposure can then be measured in adulthood. PND, postnatal day.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4226229&req=5

Figure 1: Schematic overview of the various stages of adolescence in rats. To model the effects of cannabinoid exposure at different developmental stages, rats can be treated chronically throughout the entire adolescent period (from PND28 through PND61) or during specific stages of adolescence, including early adolescence (beginning at PND28), mid-adolescence (beginning at PND38), or late adolescence (beginning at PND49). The long-term effects of adolescent cannabinoid exposure can then be measured in adulthood. PND, postnatal day.

Mentions: Animal models are useful tools for investigating the long-term behavioral effects of cannabis exposure during adolescence. To develop a suitable animal model, one must first take into consideration the obvious differences in developmental ontogeny between the animal species and human patients. Adolescence has a broad developmental border in both humans and animals. In rodents, adolescence ranges from postnatal day 28 (PND28) to PND42 (Spear, 2000), and it can be subdivided into specific phases such as early adolescence (beginning at PND28), mid-adolescence (beginning at PND38), and late adolescence (beginning at PND49) (Figure 1).


Long-term consequences of adolescent cannabinoid exposure in adult psychopathology.

Renard J, Krebs MO, Le Pen G, Jay TM - Front Neurosci (2014)

Schematic overview of the various stages of adolescence in rats. To model the effects of cannabinoid exposure at different developmental stages, rats can be treated chronically throughout the entire adolescent period (from PND28 through PND61) or during specific stages of adolescence, including early adolescence (beginning at PND28), mid-adolescence (beginning at PND38), or late adolescence (beginning at PND49). The long-term effects of adolescent cannabinoid exposure can then be measured in adulthood. PND, postnatal day.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4226229&req=5

Figure 1: Schematic overview of the various stages of adolescence in rats. To model the effects of cannabinoid exposure at different developmental stages, rats can be treated chronically throughout the entire adolescent period (from PND28 through PND61) or during specific stages of adolescence, including early adolescence (beginning at PND28), mid-adolescence (beginning at PND38), or late adolescence (beginning at PND49). The long-term effects of adolescent cannabinoid exposure can then be measured in adulthood. PND, postnatal day.
Mentions: Animal models are useful tools for investigating the long-term behavioral effects of cannabis exposure during adolescence. To develop a suitable animal model, one must first take into consideration the obvious differences in developmental ontogeny between the animal species and human patients. Adolescence has a broad developmental border in both humans and animals. In rodents, adolescence ranges from postnatal day 28 (PND28) to PND42 (Spear, 2000), and it can be subdivided into specific phases such as early adolescence (beginning at PND28), mid-adolescence (beginning at PND38), and late adolescence (beginning at PND49) (Figure 1).

Bottom Line: The endocannabinoid system plays an important role in development by acting on synaptic plasticity, neuronal cell proliferation, migration, and differentiation.Thus, over-activation of the endocannabinoid system by chronic exposure to CB1R agonists (e.g., THC, CP-55,940, and WIN55,212-2) during adolescence can dramatically alter brain maturation and cause long-lasting neurobiological changes that ultimately affect the function and behavior of the adult brain.Here, we review the relationship between cannabinoid exposure during adolescence and the increased risk of neuropsychiatric disorders, focusing on both clinical and animal studies.

View Article: PubMed Central - PubMed

Affiliation: Laboratoire de Physiopathologie des maladies Psychiatriques, UMR_S894 Institut National de la Santé et de la Recherche Médicale, Centre de Psychiatrie et Neurosciences Paris, France ; Centre Hospitalier Sainte-Anne, Service Hospitalo Universitaire, Faculté de Médecine Paris Descartes, Université Paris Descartes Paris, France.

ABSTRACT
Marijuana is the most widely used illicit drug among adolescents and young adults. Unique cognitive, emotional, and social changes occur during this critical period of development from childhood into adulthood. The adolescent brain is in a state of transition and differs from the adult brain with respect to both anatomy (e.g., neuronal connections and morphology) and neurochemistry (e.g., dopamine, GABA, and glutamate). These changes are thought to support the emergence of adult cerebral processes and behaviors. The endocannabinoid system plays an important role in development by acting on synaptic plasticity, neuronal cell proliferation, migration, and differentiation. Delta-9-tetrahydrocanabinol (THC), the principal psychoactive component in marijuana, acts as a partial agonist of the cannabinoid type 1 receptor (CB1R). Thus, over-activation of the endocannabinoid system by chronic exposure to CB1R agonists (e.g., THC, CP-55,940, and WIN55,212-2) during adolescence can dramatically alter brain maturation and cause long-lasting neurobiological changes that ultimately affect the function and behavior of the adult brain. Indeed, emerging evidence from both human and animal studies demonstrates that early-onset marijuana use has long-lasting consequences on cognition; moreover, in humans, this use is associated with a two-fold increase in the risk of developing a psychotic disorder. Here, we review the relationship between cannabinoid exposure during adolescence and the increased risk of neuropsychiatric disorders, focusing on both clinical and animal studies.

No MeSH data available.


Related in: MedlinePlus