Chronic exposure to WIN55,212-2 affects more potently spatial learning and memory in adolescents than in adult rats via a negative action on dorsal hippocampal neurogenesis

Abboussi, Oualid; Tazi, A.; Païzanis, Eleni; Ganouni, Soumaya El

doi:10.1016/j.pbb.2014.02.014

Cited by 38 publications

(31 citation statements)

References 81 publications

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“…This area warrants further investigation. Nevertheless, Abboussi et al (2014) found that chronic exposure to a CB1 agonist followed by a washout period produced no differences in HC neurogenesis in adults when compared to controls, indicating a transient effect. Conversely, when animals were exposed chronically to a CB1 agonist during adolescence, long-term reductions in HC neurogenesis were found in adulthood, indicating developmental sensitivity to a CB1 agonist exposure.…”

Section: Impact Of Adolescent Marijuana Exposure On the Hc And Behaviormentioning

confidence: 86%

The long-term cognitive consequences of adolescent exposure to recreational drugs of abuse

Mooney‐Leber

Gould

2018

Learn. Mem.

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During adolescence, the brain continues to undergo vital developmental processes. In turn, complex behavioral and cognitive skills emerge. Unfortunately, neurobiological development during adolescence can be influenced by environmental factors such as drug exposure. Engaging in drug use during adolescence has been a long-standing health concern, especially how it predicts or relates to drug using behavior later in life. However, recent findings suggest that other behavioral domains, such as learning and memory, are also vulnerable to adolescent drug use. Moreover, it is becoming increasingly apparent that deficits in learning and memory following adolescent drug use endure into adulthood, well after drug exposure has subsided. Although persistent effects suggest an interaction between drug exposure and ongoing development during adolescence, the exact acute and long-term consequences of adolescent drug exposure on substrates of learning and memory are not fully understood. Thus, this review will summarize human and animal findings on the enduring cognitive deficits due to adolescent drug exposure. Moreover, due to the fact that adolescents are more likely to consume drugs of abuse legally available to adults, this review will focus on alcohol, nicotine, and marijuana. Further, given the critical role of the frontal cortex and hippocampus in various learning and memory domains, the impact adolescent use of the previous listed drugs on the neurobiology within these regions will also be discussed.

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Section: Impact Of Adolescent Marijuana Exposure On the Hc And Behaviormentioning

confidence: 86%

The long-term cognitive consequences of adolescent exposure to recreational drugs of abuse

Mooney‐Leber

Gould

2018

Learn. Mem.

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“…This is supported by evidence that a number of BrdU + cells in the dentate gyrus are reduced in CB 2 ‐deficient mice (Palazuelos et al ., ). In contrast to this, chronic administration of another synthetic CB 1 /CB 2 agonist WIN55,212‐2 to rats during adulthood was found to have no effect on the number of immature neurons in the dentate gyrus, however, interestingly, administration during adolescence decreased the number of immature neurons, an affect that is attributed to selective suppression of dorsal but not ventral hippocampal neurogenesis (Abboussi et al ., ). Further contrasting effects are observed in the aged brain where WIN55,212‐2 administration partially restored age‐related deficits in hippocampal neurogenesis in rats (Marchalant et al ., ), suggesting a unique temporal role for cannabinoid receptors in the regulation of neurogenesis throughout the lifespan.…”

Section: In Vivo Effect Of Cannabinoids On Adult Neurogenesismentioning

confidence: 97%

The role of cannabinoids in adult neurogenesis

Prenderville

Kelly

Downer

2015

British J Pharmacology

109

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The processes underpinning post-developmental neurogenesis in the mammalian brain continue to be defined. Such processes involve the proliferation of neural stem cells and neural progenitor cells (NPCs), neuronal migration, differentiation and integration into a network of functional synapses within the brain. Both intrinsic (cell signalling cascades) and extrinsic (neurotrophins, neurotransmitters, cytokines, hormones) signalling molecules are intimately associated with adult neurogenesis and largely dictate the proliferative activity and differentiation capacity of neural cells. Cannabinoids are a unique class of chemical compounds incorporating plant-derived cannabinoids (the active components of Cannabis sativa), the endogenous cannabinoids and synthetic cannabinoid ligands, and these compounds are becoming increasingly recognized for their roles in neural developmental processes. Indeed, cannabinoids have clear modulatory roles in adult neurogenesis, probably through activation of both CB1 and CB2 receptors. In recent years, a large body of literature has deciphered the signalling networks involved in cannabinoid-mediated regulation of neurogenesis. This timely review summarizes the evidence that the cannabinoid system is intricately associated with neuronal differentiation and maturation of NPCs and highlights intrinsic/extrinsic signalling mechanisms that are cannabinoid targets. Overall, these findings identify the central role of the cannabinoid system in adult neurogenesis in the hippocampus and the lateral ventricles and hence provide insight into the processes underlying post-developmental neurogenesis in the mammalian brain. Abbreviations2-AG, 2-arachidonoylglycerol; AA, arachidonic acid; ACEA, arachidonyl-2′-chloroethylamide; AEA, anandamide; BDNF, brain-derived neurotrophic factor; BMP, bone morphogenetic protein; BrdU, 5-bromo-2'deoxyuridine; CB, cannabinoid receptor; CBC, cannabichromene; CBD, cannabidiol; CREB, cAMP response element-binding protein; DAGL, DAG lipase; DCX, double cortin; FAAH, fatty acid amide hydrolase; GFAP, glial fibrillary acidic protein; IGF-1, insulin-like growth factor-1; mTORC1, mammalian target of rapamycin complex 1; NGF, nerve-growth factor; NPC, neural progenitor cell; NSC, neural stem cell; Ptc1, patched 1; RMS, rostral migratory stream; SGZ, subgranular zone; Shh, Sonic Hedgehog; Smo, smoothened; SVZ, subventricular zone; THC, Δ IntroductionFor decades, the true plasticity of the mammalian CNS was underestimated and the adult brain was long considered to be a post-mitotic organ incapable of self-regeneration. However, pioneering work in the 1960s by Joseph Altman and colleagues challenged this long-standing dogma (Altman and Das, 1965). In this groundbreaking publication, Altman provided the first evidence that new neurons were generated in the adult rat hippocampus. Subsequent experiments demonstrated that adult neurogenesis was not specific to the hippocampus, with the adult olfactory bulb identified as another brain region where new neurons are added to existin...

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“…Investigators have only recently begun to assess underlying epigenetic modifications and its inheritance to subsequent generations. We have previously shown that chronic exposure to WIN during adolescence induces anxiety and memory deficits and decreases neuronal plasticity in rats (Abboussi et al, 2016, 2014). Also, it has been shown that chronic cannabinoid exposure in adolescent female rats increases anxiety and drug seeking behaviour in the offspring (Byrnes et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Behavioural and epigenetic effects of paternal exposure to cannabinoids during adolescence on offspring vulnerability to stress

Andaloussi

Taghzouti

Abboussi

2018

Intl J of Devlp Neuroscience

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Chronic cannabinoid exposure during adolescence in male rats induces chronic cognitive and emotional impairments. However, the impact of this form of exposure on offspring vulnerability to stress is unknown. The aim of this study was to evaluate the behavioural and epigenetic effects of stress in the offspring of male rats whose fathers were exposed to cannabinoids during adolescence. Male adolescent offspring of Win55,212‐2 (1.2 mg/kg) treated rats were exposed during one week to variable stressors and subjected to behavioural tests of anxiety and episodic‐like memory, followed by an assessment of global DNA methylation and expression of DNA methyltransferases enzymes DNMT1 and DNMT3a mRNA in the prefrontal cortex. Stress exposure induced a significant anxiogenic‐like effect but did not affect the episodic‐like memory in the offspring of Win55,212‐2 exposed fathers in comparison to the offspring of non‐exposed fathers. These behavioural changes were subsequent to a significant increase in global DNA methylation and DNMT1 and DNMTa3 transcription in the prefrontal cortex. These data suggest that the deleterious effect of chronic exposure to cannabinoids during adolescence are not limited to the exposed individuals but may increase the vulnerability to stress‐induced anxiety in the offspring and alter their epigenetic programming.

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Chronic exposure to WIN55,212-2 affects more potently spatial learning and memory in adolescents than in adult rats via a negative action on dorsal hippocampal neurogenesis

Cited by 38 publications

References 81 publications

The long-term cognitive consequences of adolescent exposure to recreational drugs of abuse

The long-term cognitive consequences of adolescent exposure to recreational drugs of abuse

The role of cannabinoids in adult neurogenesis

Behavioural and epigenetic effects of paternal exposure to cannabinoids during adolescence on offspring vulnerability to stress

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