Juvenile cannabinoid treatment induces frontostriatal gliogenesis in Lewis rats

Bortolato, Marco; Bini, Valentina; Frau, Roberto; Devoto, Paola; Pardu, Alessandra; Fan, Yijun; Solbrig, Marylou V.

doi:10.1016/j.euroneuro.2013.12.011

Cited by 30 publications

(22 citation statements)

References 59 publications

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“…These deficits were correlated with changes in basal neuronal activity (i.e., c-Fos activity) in the NAcc, amygdala, caudate putamen, and hippocampus (Wegener and Koch, 2009). In contrast, other groups reported no changes in PPI after chronically exposing adolescent rats (PND35–PND45) to THC (Bortolato et al, 2014). This discrepancy may be due to the adolescent period in which the rats were treated and/or the cannabinoid compound that was administered.…”

Section: Studying the Long-term Effects Of Cannabinoid Exposure Durinmentioning

confidence: 93%

Long-term consequences of adolescent cannabinoid exposure in adult psychopathology

et al. 2014

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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.

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Section: Studying the Long-term Effects Of Cannabinoid Exposure Durinmentioning

confidence: 93%

Long-term consequences of adolescent cannabinoid exposure in adult psychopathology

et al. 2014

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“…Secondly, the vehicle used to dissolve THC (a mixture of ethanol plus another solvent such as Cremophor) can induce behavioral side effects per se (unpublished data), while that of WIN (physiological saline with a low concentration (<3%) of Tween 20) is innocuous for mice [49]. Thirdly, WIN possesses higher affinity for cannabinoid CB1 and CB2 receptors than THC [5] and has been widely used to study the implication of the endocannabinoid system in different behaviors in rodents as well as in animal models of cannabinoid dependence [14,15,16,17,18,19,20,50]. In particular, WIN is self-administered by rodents [24,50] and induces cross-tolerance and cross-discrimination with THC [50].…”

Section: Discussionmentioning

confidence: 99%

“…Conversely, other authors have demonstrated that mice treated with WIN show an impairment in an attentional set-shifting task, supporting the notion that exposure to cannabinoids during adolescence may represent a risk factor for developing schizophrenia-like signs at adulthood [19]. Chronic pubertal WIN treatment also stimulates locomotion [17], increases novel-object exploration [18], induces depression-like behavior in the forced swim and sucrose preference tests [20] and alters anxiety-like behavior [17,20]. However, the effects of WIN on anxiety are in function of the paradigm used to evaluate anxiety.…”

Section: Introductionmentioning

confidence: 92%

“…In particular, the administration of the synthetic CB1 agonist WIN 55212-2 (WIN) to rats and mice during the adolescent period leads to long-lasting deficits in different behavioral paradigms, such as fear conditioning [14,15], progressive ratio food self-administration [16] and pre-pulse inhibition of the acoustic startle response [14,16,17]. Other authors have reported that WIN-exposed rats show only increased acoustic startle latency, but not overt deficits in sensoriomotor gating or modifications of social interaction suggesting that exposure to WIN during adolescence does not lead to psychotic-like behavior [18]. Conversely, other authors have demonstrated that mice treated with WIN show an impairment in an attentional set-shifting task, supporting the notion that exposure to cannabinoids during adolescence may represent a risk factor for developing schizophrenia-like signs at adulthood [19].…”

Section: Introductionmentioning

confidence: 99%

“…In addition, this study reports an improvement in the performance of a delay-match-to-sample working memory task in adult rats self-administering WIN during adolescence [24]. Biochemical and structural brain alterations have also been reported after adolescent treatment with WIN, such as reductions in endocannabinoid signaling and mGluR5 in the hippocampus [14], higher hippocampal anandamide levels [15], an increased turnover of striatal dopamine (but with unchanged dopamine levels) [18], higher number of active dopaminergic neurons in the ventral tegmental area [19], serotonergic hypoactivity in the dorsal raphe and noradrenergic hyperactivity in the locus coeruleus [20], impaired maturation of prefrontal GABAergic transmission [25], loss of dendritic spine density in the dentate gyrus [26], and frontostriatal gliogenesis [18]. …”

Section: Introductionmentioning

confidence: 99%

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Adolescent Exposure to the Synthetic Cannabinoid WIN 55212-2 Modifies Cocaine Withdrawal Symptoms in Adult Mice

Aguilar

Ledesma

Rodrı́guez-Arias

et al. 2017

IJMS

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Chronic cannabinoid consumption is an increasingly common behavior among teenagers and has been shown to cause long-lasting neurobehavioral alterations. Besides, it has been demonstrated that cocaine addiction in adulthood is highly correlated with cannabis abuse during adolescence. Cocaine consumption and subsequent abstinence from it can cause psychiatric symptoms, such as psychosis, cognitive impairment, anxiety, and depression. The aim of the present research was to study the consequences of adolescent exposure to cannabis on the psychiatric-like effects promoted by cocaine withdrawal in adult mice. We pre-treated juvenile mice with the cannabinoid CB1 receptor agonist WIN 55212-2 (WIN) and then subjected them to a chronic cocaine treatment during adulthood. Following these treatments, animals were tested under cocaine withdrawal in the following paradigms: pre-pulse inhibition, object recognition, elevated plus maze, and tail suspension. The long-term psychotic-like actions induced by WIN were not modified after cocaine cessation. Moreover, the memory impairments induced by cocaine withdrawal were not altered by previous adolescent WIN intake. However, WIN pre-treatment prevented the anxiogenic effects observed after cocaine abstinence, and led to greater depressive-like symptoms following cocaine removal in adulthood. This study is the first to show the long-lasting behavioral consequences of juvenile exposure to WIN on cocaine withdrawal in adult mice.

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Development of anxiety‐like behaviors during adolescence: Persistent effects of adolescent morphine exposure in male rats

Khani

Pourmotabbed

Hosseinmardi

et al. 2022

Developmental Psychobiology

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Epidemiological studies show the prevalence of opioid use, misuse and abuse in adolescents, which imposes social and economic accountability worldwide. Chronic opioid exposure, especially in adolescents, may have lasting effects on emotional behaviors that persist into adulthood. The current experiments were therefore designed to study the effects of sustained opioid exposure during adolescence on anxiety-like behaviors. Adolescent male Wistar rats underwent increasing doses of morphine for 10 days (PNDs 31-40). After that the open field test (OFT) and elevated plus maze (EPM) test were performed over a 4-week postmorphine treatment from adolescence to adulthood. Moreover, the weight of the animals was measured at these time points. We found that chronic adolescent morphine exposure reduces the weight gain during the period of morphine treatment and 4 weeks after that. It had no significant effect on the locomotor activity in the animals. Moreover, anxiolytic-like behavior was observed in the rats exposed to morphine during adolescence evaluated by OFT and EPM test.Thus, long-term exposure to morphine during adolescence has the profound potential of altering the anxiety-like behavior profile in the period from adolescence to adulthood. The maturation of the nervous system can be affected by drug abuse during the developmental window of adolescence and these effects may lead to behaviorally stable alterations.

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Juvenile cannabinoid treatment induces frontostriatal gliogenesis in Lewis rats

Cited by 30 publications

References 59 publications

Long-term consequences of adolescent cannabinoid exposure in adult psychopathology

Long-term consequences of adolescent cannabinoid exposure in adult psychopathology

Adolescent Exposure to the Synthetic Cannabinoid WIN 55212-2 Modifies Cocaine Withdrawal Symptoms in Adult Mice

Development of anxiety‐like behaviors during adolescence: Persistent effects of adolescent morphine exposure in male rats

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