Chronic URB597 treatment at adulthood reverted most depressive-like symptoms induced by adolescent exposure to THC in female rats

Realini, Natalia; Viganò, Daniela; Guidali, C.; Zamberletti, Erica; Rubino, Tiziana; Parolaro, Daniela

doi:10.1016/j.neuropharm.2010.09.003

Cited by 114 publications

(133 citation statements)

References 47 publications

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“…10,12 This leads to an adult brain characterized by altered functionality likely un derpinning cognitive impairments present in the depressive/ psychoticlike phenotype observed in female rats after ado lescent THC exposure. 10,11 Thus, hindering the first event (the increase in Suv39H1/H3K9me3) through chaetocin adminis tration, we prevented, at least in part, the flow of events that lead to impairments in brain and behaviour (Fig. 10).…”

Section: Discussionmentioning

confidence: 99%

“…Because the onset of the depressive/psychoticlike pheno type is restricted to adolescent THC exposure, [8][9][10][11][12][13][14] we investi gated whether described alterations in histone modifications and gene expression were restricted to the adolescent treat ment. We performed the same protocol of injections (Fig.…”

Section: Adult V Adolescent Thc Exposure Differentially Affects Histmentioning

confidence: 99%

“…To investigate the possible role of H3K9me3 increase induced by adolescent THC exposure, [8][9][10][11][12][13] we administered chaetocin, an inhibitor of the HMTs SUV39H1 and G9a, 34,35 simultane ously with THC treatment. To establish the active dose of chaetocin in vivo, we first tested 2 different intraperitoneal doses (0.05 mg/kg and 0.1 mg/kg), and 24 hours after the in jection, we investigated H3K9me3 levels.…”

Section: Chaetocin-induced H3k9me3 Inhibition During Adolescent Thc Ementioning

confidence: 99%

“…[5][6][7] We have shown previously that chronic admin istration of Δ9tetrahydrocannabinol (THC), the psychoactive ingredient of cannabis, in adolescent but not adult female rats induces behavioural and biochemical signs relevant for de pression and psychosis [8][9][10][11][12][13] later in life. Interestingly, long term effects of THC seem to be sexspecific.…”

Section: Introductionmentioning

confidence: 99%

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Adolescent THC exposure in female rats leads to cognitive deficits through a mechanism involving chromatin modifications in the prefrontal cortex

Prini

Rusconi

Zamberletti

et al. 2018

jpn

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Section: Discussionmentioning

confidence: 99%

Section: Adult V Adolescent Thc Exposure Differentially Affects Histmentioning

confidence: 99%

Section: Chaetocin-induced H3k9me3 Inhibition During Adolescent Thc Ementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Adolescent THC exposure in female rats leads to cognitive deficits through a mechanism involving chromatin modifications in the prefrontal cortex

Prini

Rusconi

Zamberletti

et al. 2018

jpn

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“…High doses usually induce anxiogenic-like responses in rodents (490,755). Chronic exposure to ⌬ 9 -THC in adolescent rats induces a depressive-like phenotype in adulthood (720,756). In humans, the interindividual variability in the responses to cannabis may depend on a wide spectrum of factors, such as the relative concentrations of ⌬ 9 -THC and other phytocannabinoids (846).…”

mentioning

confidence: 99%

From Phytocannabinoids to Cannabinoid Receptors and Endocannabinoids: Pleiotropic Physiological and Pathological Roles Through Complex Pharmacology

Ligresti¹,

Petrocellis²,

Marzo³

2016

Physiological Reviews

365

337

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Apart from having been used and misused for at least four millennia for, among others, recreational and medicinal purposes, the cannabis plant and its most peculiar chemical components, the plant cannabinoids (phytocannabinoids), have the merit to have led humanity to discover one of the most intriguing and pleiotropic endogenous signaling systems, the endocannabinoid system (ECS). This review article aims to describe and critically discuss, in the most comprehensive possible manner, the multifaceted aspects of 1) the pharmacology and potential impact on mammalian physiology of all major phytocannabinoids, and not only of the most famous one ⌬ 9 -tetrahydrocannabinol, and 2) the adaptive prohomeostatic physiological, or maladaptive pathological, roles of the ECS in mammalian cells, tissues, and organs. In doing so, we have respected the chronological order of the milestones of the millennial route from medicinal/recreational cannabis to the ECS and beyond, as it is now clear that some of the early steps in this long path, which were originally neglected, are becoming important again. The emerging picture is rather complex, but still supports the belief that more important discoveries on human physiology, and new therapies, might come in the future from new knowledge in this field.

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Sex, drugs, and adult neurogenesis: Sex‐dependent effects of escalating adolescent cannabinoid exposure on adult hippocampal neurogenesis, stress reactivity, and amphetamine sensitization

et al. 2013

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Cannabinoid exposure during adolescence has adverse effects on neuroplasticity, emotional behavior, cognition, and reward sensitivity in adult rats. We investigated whether escalating doses of the cannabinoid receptor 1 (CB1 R) agonist, HU-210, in adolescence would affect adult hippocampal neurogenesis and behavioral processes putatively modulated by hippocampal neurogenesis, in adult male and female Sprague-Dawley rats. Escalating doses of HU-210 (25, 50, and 100 µg/kg), or vehicle were administered from postnatal day (PND) 35 to 46. Animals were left undisturbed until PND 70, when they were treated with 5-bromo-2-deoxyuridine (BrdU; 200 mg/kg) and perfused 21 days later to examine density of BrdU-ir and BrdU/NeuN cells in the dentate gyrus. In another cohort, hypothalamic-pituitary-adrenal (HPA) axis reactivity to an acute restraint stress (30 min; PND 75) and behavioral sensitization to d-amphetamine sulfate (1-2 mg/kg; PND 105-134) were assessed in adulthood. Adolescent HU-210 administration suppressed the density of BrdU-ir cells in the dentate gyrus in adult male, but not adult female rats. Adolescent HU-210 administration also induced significantly higher peak corticosterone levels and reminiscent of the changes in neurogenesis, this effect was more pronounced in adult males than females. However, adolescent cannabinoid treatment resulted in significantly higher stereotypy scores in adult female, but not male, rats. Thus, adolescent CB1 R activation suppressed hippocampal neurogenesis and increased stress responsivity in adult males, but not females, and enhanced amphetamine sensitization in adult female, but not male, rats. Taken together, increased CB1 R activation during adolescence results in sex-dependent, long-term, changes to hippocampal structure and function, an effect that may shed light on differing vulnerabilities to developing disorders following adolescent cannabinoid exposure, based on sex.

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Chronic URB597 treatment at adulthood reverted most depressive-like symptoms induced by adolescent exposure to THC in female rats

Cited by 114 publications

References 47 publications

Adolescent THC exposure in female rats leads to cognitive deficits through a mechanism involving chromatin modifications in the prefrontal cortex

Adolescent THC exposure in female rats leads to cognitive deficits through a mechanism involving chromatin modifications in the prefrontal cortex

From Phytocannabinoids to Cannabinoid Receptors and Endocannabinoids: Pleiotropic Physiological and Pathological Roles Through Complex Pharmacology

Sex, drugs, and adult neurogenesis: Sex‐dependent effects of escalating adolescent cannabinoid exposure on adult hippocampal neurogenesis, stress reactivity, and amphetamine sensitization

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