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α‐noradrenergic receptor modulation of the phencyclidine‐ and Δ 9 ‐tetrahydrocannabinol‐induced increases in dopamine utilization in rat prefrontal cortex
Author(s) -
Jentsch J. David,
Wise Alyssa,
Katz Zachary,
Roth Robert H.
Publication year - 1998
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/(sici)1098-2396(199801)28:1<21::aid-syn3>3.0.co;2-e
Subject(s) - phencyclidine , prefrontal cortex , dopamine , neuroscience , tetrahydrocannabinol , chemistry , modulation (music) , receptor , psychology , nmda receptor , cannabinoid , cognition , biochemistry , physics , acoustics
The noncompetitive NMDA receptor antagonist phencyclidine (PCP) and the neuronal cannabinoid receptor agonist Δ 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 α‐noradrenergic receptors on PCP‐ and THC‐induced increases in prefrontal cortical and nucleus accumbens dopamine utilization in the rat were examined. Clonidine, an α 2 noradrenergic receptor agonist, completely blocked the activation of mesoprefrontal dopamine system by THC or PCP. In addition, the α 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. Synapse 28:21–26, 1998. © 1998 Wiley‐Liss, Inc.