Behavioural disturbances and altered Fos protein expression in adult rats after chronic pubertal cannabinoid treatment

Wegener, Nico; Koch, Michael

doi:10.1016/j.brainres.2008.11.081

Cited by 85 publications

(66 citation statements)

References 69 publications

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“…However, due to the site-specific nature of cannabinoid application, it is difficult to predict the directionality of the effects of THC on anxiety behaviour, given our systemic application in adolescence. Some similar studies have observed increases [24,66], no change [28] or decreases [67] in anxiety following chronic cannabinoid administration during the adolescent period. Therefore, although our results do not fit into the conception of adverse effects of THC on anxiety behaviour, our results do agree with other researchers who have shown either no effects or decreased anxiety behaviour.…”

Section: Effects Of Thcmentioning

confidence: 85%

Part II: Strain- and sex-specific effects of adolescent exposure to THC on adult brain and behaviour: Variants of learning, anxiety and volumetric estimates

Keeley

Trow

Bye

et al. 2015

Behavioural Brain Research

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Section: Effects Of Thcmentioning

confidence: 85%

Part II: Strain- and sex-specific effects of adolescent exposure to THC on adult brain and behaviour: Variants of learning, anxiety and volumetric estimates

Keeley

Trow

Bye

et al. 2015

Behavioural Brain Research

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“…Acutely, cannabinoid agonists can induce anxiolytic-like effects at lower doses and anxiogenic-like effects at higher doses, in a manner that can differ between adolescent and adult animals (Viveros et al, 2005a, ). Rodent models of chronic exposure across diverse paradigms have produced conflicting results, with studies reporting anxietylike behavior to be decreased, particularly using the EPM (Biscaia et al, 2003;Schramm-Sapyta et al, 2007;Wegener and Koch, 2009), unaltered (Rubino et al, 2009) or increased (O'Shea et al, 2004(O'Shea et al, , 2006. In humans, adolescent cannabis exposure has been associated with depressive and/or anxiety disorders, in addition to psychosis (Patton et al, 2002).…”

Section: Anxietymentioning

confidence: 98%

Chronic Adolescent Exposure to Δ-9-Tetrahydrocannabinol in COMT Mutant Mice: Impact on Psychosis-Related and Other Phenotypes

O’Tuathaigh

Hryniewiecka

Behan

et al. 2010

Neuropsychopharmacol

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Cannabis use confers a two-fold increase in the risk for psychosis, with adolescent use conferring even greater risk. A high-low activity catechol-O-methyltransferase (COMT ) polymorphism may modulate the effects of adolescent D-9-tetrahydrocannabinol (THC) exposure on the risk for adult psychosis. Mice with knockout of the COMT gene were treated chronically with THC (4.0 and 8.0 mg/kg over 20 days) during either adolescence (postnatal days (PDs) 32-52) or adulthood (PDs 70-90). The effects of THC exposure were then assessed in adulthood across behavioral phenotypes relevant for psychosis: exploratory activity, spatial working memory (spontaneous and delayed alternation), object recognition memory, social interaction (sociability and social novelty preference), and anxiety (elevated plus maze). Adolescent THC administration induced a larger increase in exploratory activity, greater impairment in spatial working memory, and a stronger anti-anxiety effect in COMT knockouts than in wild types, primarily among males. No such effects of selective adolescent THC administration were evident for other behaviors. Both object recognition memory and social novelty preference were disrupted by either adolescent or adult THC administration, independent of genotype. The COMT genotype exerts specific modulation of responsivity to chronic THC administration during adolescence in terms of exploratory activity, spatial working memory, and anxiety. These findings illuminate the interaction between genes and adverse environmental exposures over a particular stage of development in the expression of the psychosis phenotype.

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“…Molecular signatures of compromised synaptic efficacy have been reported in the PFC (Rubino et al, 2009a), along with abnormalities in Akt, Wnt, and mTOR signaling cascades that “bear… remarkable similarity to adaptations observed in neuropsychiatric populations” (Renaud et al, 2016, p. 2). Adolescent CB exposure has also been reported to disrupt regulation of transcription factors induced by DA manipulations in the AMYG, and to alter receptor expression, transcription factors, opiate- and CB-sensitive signaling cascades and immediate early gene expression in forebrain DA terminal regions such as the nAc (Ellgren et al, 2008; Rubino et al, 2008; Wegener & Koch 2009). Although many of the molecular studies to date have focused only on consequences of adolescent exposures, in recent studies where exposure age has been varied, the adolescent brain has been shown to be either particularly vulnerable or to reveal different persisting alterations following repeated CB exposure than that observed in the adult brain (e.g., see Renaud et al, 2016).…”

Section: Cannabinoidsmentioning

confidence: 99%

Consequences of adolescent use of alcohol and other drugs: Studies using rodent models

Spear

2016

Neuroscience & Biobehavioral Reviews

140

112

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Studies using animal models of adolescent exposure to alcohol, nicotine, cannabinoids, and the stimulants cocaine, 3,4-Methylenedioxymethampethamine and methamphetamine have revealed a variety of persisting neural and behavioral consequences. Affected brain regions often include mesolimbic and prefrontal regions undergoing notable ontogenetic change during adolescence, although it is unclear whether this represents areas of specific vulnerability or particular scrutiny to date. Persisting alterations in forebrain systems critical for modulating reward, socioemotional processing and cognition have emerged, including apparent induction of a hyper-dopaminergic state with some drugs and/or attenuations in neurons expressing cholinergic markers. Disruptions in cognitive functions such as working memory, alterations in affect including increases in social anxiety, and mixed evidence for increases in later drug self-administration have also been reported. When consequences of adolescent and adult exposure were compared, adolescents were generally found to be more vulnerable to alcohol, nicotine, and cannabinoids, but generally not to stimulants. More work is needed to determine how adolescent drug exposure influences sculpting of the adolescent brain, and provide approaches to prevent/reverse these effects.

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Behavioural disturbances and altered Fos protein expression in adult rats after chronic pubertal cannabinoid treatment

Cited by 85 publications

References 69 publications

Part II: Strain- and sex-specific effects of adolescent exposure to THC on adult brain and behaviour: Variants of learning, anxiety and volumetric estimates

Part II: Strain- and sex-specific effects of adolescent exposure to THC on adult brain and behaviour: Variants of learning, anxiety and volumetric estimates

Chronic Adolescent Exposure to Δ-9-Tetrahydrocannabinol in COMT Mutant Mice: Impact on Psychosis-Related and Other Phenotypes

Consequences of adolescent use of alcohol and other drugs: Studies using rodent models

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