α-noradrenergic receptor modulation of the phencyclidine- and Δ9-tetrahydrocannabinol-induced increases in dopamine utilization in rat prefrontal cortex
✍ Scribed by J. David Jentsch; Alyssa Wise; Zachary Katz; Robert H. Roth
- Publisher
- John Wiley and Sons
- Year
- 1998
- Tongue
- English
- Weight
- 75 KB
- Volume
- 28
- Category
- Article
- ISSN
- 0887-4476
No coin nor oath required. For personal study only.
✦ Synopsis
The noncompetitive NMDA receptor antagonist phencyclidine (PCP) and the neuronal cannabinoid receptor agonist ⌬ 9 -tetrahydrocannabinol (THC) are two agents shown to have psychotomimetic properties in humans. Both drugs increase dopamine release and utilization in the prefrontal cortex, a brain region thought to be dysfunctional in schizophrenia. In the present series of studies, the effects of drugs acting at ␣-noradrenergic receptors on PCP-and THC-induced increases in prefrontal cortical and nucleus accumbens dopamine utilization in the rat were examined. Clonidine, an ␣ 2 noradrenergic receptor agonist, completely blocked the activation of mesoprefrontal dopamine system by THC or PCP. In addition, the ␣ 1 noradrenergic receptor antagonist prazosin blocked the PCP-induced increase in prefrontal cortical dopamine utilization. These data may provide new insights concerning pharmacological therapies for acute drug-induced psychoses and behavioral abnormalities in human PCP and THC abusers.