Neuroscience 2002 Abstract
| Presentation Number: | 674.14 |
|---|---|
| Abstract Title: | CHRONIC Δ-9-TETRAHYDROCANNABINOL EXPOSURE INDUCES PERSISTENT ATTENTIONAL DEFICITS. |
| Authors: |
Verrico, C. D.*1
; Jentsch, J. D.3
; Roth, R. H.1,2
; Taylor, J. R.2
1Pharmacology, Yale Univ, New Haven, CT 2Psychiatry, Yale Univ, New Haven, CT 3Psychology, University of California at Los Angeles, Los Angeles, CA |
| Primary Theme and Topics |
Cognition and Behavior - Animal Cognition and Behavior -- Attention |
| Session: |
674. Animal cognition and behavior: attention Poster |
| Presentation Time: | Wednesday, November 6, 2002 9:00 AM-10:00 AM |
| Location: | Hall A2-B3 N-25 |
| Keywords: | CANNABINOIDS, ATTENTION, DRUG ABUSE, PREFRONTAL CORTEX |
The abuse of Δ-9-tetrahydrocannabinol (THC), the principal psychoactive constituent of marijuana, is associated with persistent cognitive dysfunction. We therefore studied the effects of chronic administration of THC (10 mg/kg) on cognitive function in the rat. THC administration, twice daily for 14 days, resulted in a persistent attentional impairment that is reminiscent of cognitive deficits observed following excitotoxic lesions of the dorsomedial frontal cortex. Specifically, rats chronically administered THC showed subsequent impairments in a self-paced version of the classic 5-choice serial reaction time task, which persisted 14 days after the final drug administration. Longer time points have yet to be examined. These attentional impairments were temporarily reversible by an acute amphetamine (0.5 mg/kg) challenge. Importantly, the attentional deficit was observed after withdrawal from THC, suggesting that the behavioral effects were drug-induced changes in the brain rather than a direct effect of THC. These behavioral data demonstrate that chronic THC administration to rats induces an attentional deficit, similar to that observed in humans who heavily abuse marijuana. Moreover, these THC-induced attentional impairments were associated with neurochemical deficits in cortical dopamine and acetylcholine activity. Finally, amphetamine’s ability to reverse the attentional impairments provides indirect evidence that the observed cortical dopaminergic and cholinergic deficits may be linked to the cognitive dysfunction.
Supported, in part, by grants DA 11717 and MH 14092.
Supported, in part, by grants DA 11717 and MH 14092.
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2002 Neuroscience Meeting Planner. Orlando, FL: Society for Neuroscience, 2002. Online.
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