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Repeated, intermittent delta(9)-tetrahydrocannabinol administration to rats impairs acquisition and performance of a test of visuospatial divided attention.

Christopher D. Verrico, J David Jentsch, Robert H Roth, Jane R. Taylor

Neuropsychopharmacology March 2004 DOI: 10.1038/sj.npp.1300316 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Controlled experimental animal study Peer reviewed
Population Rats
Interventions Delta(9)-tetrahydrocannabinol (THC) Amphetamine
Dose THC 10.0 mg/kg twice daily; amphetamine 0.5 mg/kg
Duration 14 days of THC administration; follow-up 14 days after the final dose
Measures lateralized reaction time task (self-paced version of the multiple-choice serial reaction time task)
Topics Cannabis
Key findings Rats given subchronic THC (10.0 mg/kg twice daily for 14 days) showed impairments on a lateralized reaction time task that persisted 14 days after the final dose; an acute amphetamine challenge (0.5 mg/kg) transiently reversed the deficit. The authors conclude chronic THC induces an attentional deficit in rats similar to that in humans who abuse marijuana, and suggest monoaminergic deficits may contribute.

Abstract

The residual neuropsychological effects of marijuana abuse in man indicate a dysfunction of the attentional/executive systems. Moreover, experimental investigations suggest that repeated, intermittent (subchronic) Delta(9)-tetrahydrocannabinol (THC), the main psychoactive ingredient of marijuana, alters neurotransmission in the frontal cortex of rats and humans, a key neural site mediating attention and executive functions. In the present studies, the acquisition and performance of a test of visuospatial attention (the lateralized reaction time task) after subchronic THC administration (10.0 mg/kg twice daily for 14 days) was examined. Rats previously administered THC showed impairments in this self-paced version of the classic multiple-choice serial reaction time task, which persisted 14 days after the final drug administration. Longer time points were not examined. These attentional impairments were transiently reversible with an acute amphetamine (0.5 mg/kg) challenge. These behavioral data demonstrate that chronic THC administration to rats induces an attentional deficit, similar to that observed in humans who abuse marijuana. Finally, amphetamine's ability to reverse the attentional impairments provides indirect evidence that monoaminergic deficits may be linked to the cognitive dysfunction.

Comparable studies

Other preclinical and animal studies on cannabis, most cited first.

Study Year Design Participants
Cognitive Impairment Induced by Delta9-tetrahydrocannabinol Occurs through Heteromers between Cannabinoid CB1 and Serotonin 5-HT2A Receptors Mice 2015 Preclinical study
Interaction of drugs of abuse and maintenance treatments with human P-glycoprotein (ABCB1) and breast cancer resistance protein (ABCG2). hMDR1- and hBCRP-transfected HEK293 cells and hMDR1- and hBCRP-MDCKII cells 2010 In vitro study
Long-term hippocampal interneuronopathy drives sex-dimorphic spatial memory impairment induced by prenatal THC exposure Mice prenatally exposed to THC, including conditional CB1R knockout mice 2020 Animal experimental study
Chronic cannabis promotes pro-hallucinogenic signaling of 5-HT2A receptors through Akt/mTOR pathway Mice exposed to chronic THC early in life 2018 Animal experimental study
Effects of cannabinoid drugs on the deficit of prepulse inhibition of startle in an animal model of schizophrenia: the SHR strain Spontaneously hypertensive rats (SHRs) and Wistar rats 2014 Animal experimental study

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