Delta 9-tetrahydrocannabinol increases prefrontal cortical catecholaminergic utilization and impairs spatial working memory in the rat: blockade of dopaminergic effects with HA966.
J D Jentsch, E Andrusiak, A Tran, M B Bowers, R H Roth
Neuropsychopharmacology June 1997 DOI: 10.1016/s0893-133x(97)00018-3 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Experimental study Peer reviewed |
|---|---|
| Population | Rats |
| Interventions | THC HA966 |
| Dose | 5 mg/kg i.p. THC |
| Topics | Cannabis |
| Key findings | THC (5 mg/kg i.p.) increased dopamine and norepinephrine turnover in the prefrontal cortex and impaired spatial working memory in rats. HA966 enantiomers prevented the dopamine increase and partially blocked norepinephrine elevation, while also ameliorating the memory impairment. |
Abstract
The present study examined delta 9-tetrahydrocannabinol (THC)-induced alterations in monoamine transmission in the rat forebrain as well as the effects of the enantiomers of 3-amino-1-hydroxypyrrolid-2-one (HA966) on the monoamine response to THC. Activation of dopamine (DA) and norepinephrine (NE) but not serotonin (5-HT) turnover in the prefrontal cortex (PFC) was observed after THC (5 mg/kg i.p.) administration. Both enantiomers of HA966 completely prevented the effects of THC on PFC DA turnover and partially blocked the THC-induced rise in NE metabolism. The cognitive consequences of THC exposure were also examined. THC significantly impaired spatial working, but not reference, memory in rats, and this effect was ameliorated by HA966. Thus, HA966 prevents the THC-induced increases in PFC DA turnover and impairments of prefrontal cortical working memory function. Furthermore, these data suggest that cognitive impairments displayed by marijuana self-administering humans may be related to PFC DA hyperactivity and that HA966 may prevent this effect.
Comparable studies
Other preclinical and animal studies on cannabis, most cited first.
Citations in the library
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