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George R. Breese, Ph.D.

Professor
Email: gbreese@med.unc.edu
Office Phone: 919-966-3081
http://www.med.unc.edu/alcohol/faculty/BreeseGR/Breese.htm
 

Education:
B.S., Pharmacy: Butler University
M.S., Pharmacology; Minor, Medicinal Chemistry: Butler University
Ph.D., Pharmacology; Minor, Physiology: University of Tennessee


Summary Statement:
The Neuropharmacology laboratory, which Dr. Breese directs, has as a primary mission to understand the persistent effects of lesions to neural systems and the neural consequences of chronic administration of drugs. Currently, the laboratory is investigating the neurochemical and neuroanatomical basis of the sensitization of anxiety-like behavior induced by repeated withdrawals from 3 cycles of chronic ethanol exposure. Furthermore, there is an effort to understand the basis of stress substituting for withdrawals from chronic ethanol to sensitize withdrawal-induced deficits in anxiety and to increase voluntary drinking. In rats with dopamine-containing neurons destroyed during development to model the dopamine loss in Lesch-Nyhan disease, work continues to understand the basis of priming of the sensitivity of responses to D1-dopamine agonists in rats lesioned as neonates by exploring chronic changes in transcription factors. Since the neonate-lesioned rat may also serve as a model of NMDA hypofunction in schizophrenia because of its supersensitivity to repeated treatment with NMDA antagonists, the neurochemical and neuroanatomical basis of this behavioral sensitization to NMDA antagonists is sought.

Representative Publications:
1. Breese GR, Baumeister AA, McCown TJ, Emerick SG, Frye GD, Crotty K, Mueller RA: Behavioral differences between neonatal and young adult 6-hydroxydopamine-treated rats to dopamine agonists: Relevance to neurological symptoms in clinical syndromes with reduced brain dopamine. J Pharmacol Exp Ther 231:343-354, 1984.

2. Criswell, H.E., Mueller, R.A. and Breese, G.R.: Long-term D1-dopamine receptor sensitization in neonatal-6-OHDA-lesioned rats is blocked by an NMDA antagonist. Brain Res. 512:284-290, 1990.

3. Breese, G.R., Knapp, D.J., and Moy, S.S., Integrative role for serotonergic and gluatmatergic receptor mechanisms in the action of NMDA antagonists: Potential relationships to acute and chronic actions of antipsychotic drugs. Neuroscience and Biobehavioral Reviews 26:441-455, 2002

4. Overstreet, D.H., Knapp, D.J., and Breese, G.R. Accentuated decrease in social interaction in rats subjected to multiple alcohol withdrawals. Alcoholism: Clin. Exp. Res. 26:1259-1268, 2002

5. Moy, S.S. and Breese, G.R. Phencylidine supersensitivity in rats with neonatal dopamine loss. Psychopharmacology 161:255-262, 2002.




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