Cannabis ‐ 1988

Hollister, Leo E.

doi:10.1111/j.1600-0447.1988.tb08576.x

Cited by 45 publications

(12 citation statements)

References 59 publications

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“…Cannabis contains other cannabinoids (e.g., cannabidiol), as well as terpenoids and flavonoids (47), some of which could enhance or offset the effects of THC (48, 49). …”

Section: Discussionmentioning

confidence: 99%

Repeated Δ⁹-Tetrahydrocannabinol Exposure in Adolescent Monkeys: Persistent Effects Selective for Spatial Working Memory

Verrico¹,

Gu²,

Peterson³

et al. 2014

AJP

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Objective Epidemiological findings suggest that, relative to adults, adolescents are more vulnerable to the adverse persistent effects of cannabis on working memory. However, the potential confounds inherent in human studies preclude direct determination of a cause-and-effect relationship between adolescent cannabis use and heightened susceptibility to persistent working memory impairments. Consequently, the authors examined the effects of repeated exposure to Δ9-tetrahydrocannabinol (THC) on performance of spatial and object working memory tasks in adolescent monkeys. Method Seven pairs of male adolescent rhesus monkeys, matched for baseline cognitive performance, received vehicle or THC intravenously 5 days/week for 6 months. Performance on spatial and object memory tasks was assessed 23 or 71 hours after drug administration throughout the study. In addition, acute effects on working memory were also assessed at the beginning and end of the 6-month period. Results Relative to the vehicle-exposed control animals, those with repeated THC exposure had a blunted trajectory of accuracy improvements on the spatial working memory task in a delay-dependent manner. Accuracy improvements on the object working memory task did not differ between groups. Relative to the acute effects of THC on working memory at the beginning of the study, neither sensitivity nor tolerance was evident after 6 months of THC exposure. Conclusions Because maturation of performance is later for spatial than for object working memory, these findings suggest that persistent effects of THC on cognitive abilities are more evident when exposure coincides with the developmental stage during which the underlying neural circuits are actively maturing.

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“…Cannabis contains other cannabinoids (e.g., cannabidiol), as well as terpenoids and flavonoids (47), some of which could enhance or offset the effects of THC (48, 49). …”

Section: Discussionmentioning

confidence: 99%

Repeated Δ⁹-Tetrahydrocannabinol Exposure in Adolescent Monkeys: Persistent Effects Selective for Spatial Working Memory

Verrico¹,

Gu²,

Peterson³

et al. 2014

AJP

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“…In contrast, some studies suggest that schizophrenia patients who use cannabis have fewer negative symptoms compared to those who do not (155, 156). This evidence, however, is limited due to the cross-sectional design of these studies.…”

Section: Cannabis and Cognitive And Negative Symptomsmentioning

confidence: 98%

Impact of Cannabis Use on the Development of Psychotic Disorders

2014

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The link between cannabis use and psychosis comprises three distinct relationships: acute psychosis associated with cannabis intoxication, acute psychosis that lasts beyond the period of acute intoxication, and persistent psychosis not time-locked to exposure. Experimental studies reveal that cannabis, tetrahydrocannabinol (THC) and synthetic cannabinoids reliably produce transient positive, negative, and cognitive symptoms in healthy volunteers. Case-studies indicate that cannabinoids can induce acute psychosis which lasts beyond the period of acute intoxication but resolves within a month. Exposure to cannabis in adolescence is associated with a risk for later psychotic disorder in adulthood; this association is consistent, temporally related, shows a dose-response, and is biologically plausible. However, cannabis is neither necessary nor sufficient to cause a persistent psychotic disorder. More likely it is a component cause that interacts with other factors to result in psychosis. The link between cannabis and psychosis is moderated by age at onset of cannabis use, childhood abuse and genetic vulnerability. While more research is needed to better characterize the relationship between cannabinoid use and the onset and persistence of psychosis, clinicians should be mindful of the potential risk of psychosis especially in vulnerable populations, including adolescents and those with a psychosis diathesis.

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“…The nosological status of the syndrome is, however, debated. Further, the confounding effects of concomitant poly-substance abuse, poverty, low socio-economic status, or pre-existing psychiatric disorders may explain the association (214, 215). …”

Section: Delayed and Persistent Effects Of Cannabinoidsmentioning

confidence: 99%

Gone to Pot â€“ A Review of the Association between Cannabis and Psychosis

2014

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Cannabis is the most commonly used illicit drug worldwide, with ~5 million daily users worldwide. Emerging evidence supports a number of associations between cannabis and psychosis/psychotic disorders, including schizophrenia. These associations-based on case-studies, surveys, epidemiological studies, and experimental studies indicate that cannabinoids can produce acute, transient effects; acute, persistent effects; and delayed, persistent effects that recapitulate the psychopathology and psychophysiology seen in schizophrenia. Acute exposure to both cannabis and synthetic cannabinoids (Spice/K2) can produce a full range of transient psychotomimetic symptoms, cognitive deficits, and psychophysiological abnormalities that bear a striking resemblance to symptoms of schizophrenia. In individuals with an established psychotic disorder, cannabinoids can exacerbate symptoms, trigger relapse, and have negative consequences on the course of the illness. Several factors appear to moderate these associations, including family history, genetic factors, history of childhood abuse, and the age at onset of cannabis use. Exposure to cannabinoids in adolescence confers a higher risk for psychosis outcomes in later life and the risk is dose-related. Individuals with polymorphisms of COMT and AKT1 genes may be at increased risk for psychotic disorders in association with cannabinoids, as are individuals with a family history of psychotic disorders or a history of childhood trauma. The relationship between cannabis and schizophrenia fulfills many but not all of the standard criteria for causality, including temporality, biological gradient, biological plausibility, experimental evidence, consistency, and coherence. At the present time, the evidence indicates that cannabis may be a component cause in the emergence of psychosis, and this warrants serious consideration from the point of view of public health policy.

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Cannabis ‐ 1988

Cited by 45 publications

References 59 publications

Repeated Δ⁹-Tetrahydrocannabinol Exposure in Adolescent Monkeys: Persistent Effects Selective for Spatial Working Memory

Repeated Δ⁹-Tetrahydrocannabinol Exposure in Adolescent Monkeys: Persistent Effects Selective for Spatial Working Memory

Impact of Cannabis Use on the Development of Psychotic Disorders

Gone to Pot â€“ A Review of the Association between Cannabis and Psychosis

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Cannabis ‐ 1988

Cited by 45 publications

References 59 publications

Repeated Δ9-Tetrahydrocannabinol Exposure in Adolescent Monkeys: Persistent Effects Selective for Spatial Working Memory

Repeated Δ9-Tetrahydrocannabinol Exposure in Adolescent Monkeys: Persistent Effects Selective for Spatial Working Memory

Impact of Cannabis Use on the Development of Psychotic Disorders

Gone to Pot â€“ A Review of the Association between Cannabis and Psychosis

Contact Info

Product

Resources

About

Repeated Δ⁹-Tetrahydrocannabinol Exposure in Adolescent Monkeys: Persistent Effects Selective for Spatial Working Memory

Repeated Δ⁹-Tetrahydrocannabinol Exposure in Adolescent Monkeys: Persistent Effects Selective for Spatial Working Memory