Neuroscience 2002 Abstract
| Presentation Number: | 674.15 |
|---|---|
| Abstract Title: | CHRONIC EXPOSURE TO CANNABINOIDS DECREASES PREFRONTAL CORTICAL DOPAMINE TURNOVER AND ACETYLCHOLINE RELEASE IN THE RAT. |
| Authors: |
Roth, R. H.*1,2
; Jentsch, J. D.3
; Verrico, C. D.1
1Pharmacology, Yale Univ Sch Med, New Haven, CT 2Psychiatry, Yale Univ Sch Med, New Haven, CT 3Psychology, University of 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 10:00 AM-11:00 AM |
| Location: | Hall A2-B3 N-25 |
| Keywords: | CANNABINOIDS, PREFRONTAL CORTEX, ACETYLCHOLINE, DOPAMINE |
Abuse of Δ-9-tetrahydrocannabinol (THC), the major psychoactive ingredient of marijuana, induces persistent cognitive deficits (especially of memory and attention) reminiscent of prefrontal cortical dysfunction in humans. Dopamine and acetylcholine are critical transmitters in the memory and attentional processes of the prefrontal cortex. Preliminary findings from our lab suggest that repeated administration of THC to rats reduces frontal cortical dopamine turnover. Given that these alterations of cortical dopamine may be related to the cognitive deficits induced by chronic THC exposure, we extended the findings on dopamine turnover. Furthermore, we utilized in vivo microdialysis to assess the consequences of chronic exposure to cannabinoid agonists on basal and evoked acetylcholine release in the rat prefrontal cortex. Chronic exposure to THC or WIN 55,212-2 (10 mg/kg, twice daily for 7 or 14 days) caused a selective and persistent reduction in medial prefrontal cortical dopamine turnover and basal extracellular concentrations of acetylcholine release. These cannabinoid-induced dopaminergic and cholinergic deficits were maintained in the prefrontal cortex after a withdrawal period. As such, the neurochemical effects are arguably due to drug-induced neurobiological changes rather than persistent drug interactions with cannabinoid receptors. Thus, the cognitive/attentional impairments associated with long-term cannabis use may be subserved by drug-induced alterations in frontal cortical dopamine and acetylcholine transmission.
Supported by grant MH 14092.
Supported by grant 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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