Faculty & Research

Preclinical Neuropsychopharmacology Research Team

Breese Lab (Left to Right): George Breese, Ph.D., Kui-Ling Huang, Darin Knapp, Ph.D., Yan Hua Gao, MD, David Overstreet, Ph.D., Katie Jungbluth, Bonita Blake, DVM, Ph.D., Hugh Criswell, Ph.D., Zhen Ming, MD, Chris Halloran, Bob Angel, Montse Navarro, Ph.D., Alia Dickinson, Tiffany Wills, Thomas McCown, Ph.D.

Our Focus

The primary focus of our laboratory is to understand adaptive changes in brain that accompany prolonged drug treatment and lesions to specific neural systems in brain. There are three areas of research which allow the laboratory to maintain the aim of the laboratory. One is an investigation of the adaptive mechanisms that accompany neonatal destruction of dopaminergic neurons. This particular treatment is important because it models the dopamine deficiency observed in Lesch-Nyhan disease.

A variety of techniques are used to evaluate this model including behavioral, pharmacological, electrophysiological, biochemical and anatomical approaches. The second major area of interest is the study of the acute and chronic actions of ethanol on brain function. This work assesses the sedative, anticonflict and seizure producing properties of ethanol.

Multidisciplinary approaches are used to evaluate these actions of ethanol on GABA and NMDA neural mechanisms including anatomical, molecular biological,behavioral and electrophysiological methods. Finally, the laboratory is working to define the site within brain where antidepressant drugs act to effect corticoid release and anxiety present in depression. This latter work utilizes chemical, anatomical and behavioral approaches to define the adaptive changes that accompany chronic antidepressant treatment.

Research Contributions

--Discovered that ethanol has selective actions on receptor subtypes of ligand-gated ion channels which has a molecular basis and is related to brain regional differences in sensitivity to alcohol.

--Identified the medial septum as a key area in brain responsible for ethanol-induced sedation.

--Found that TRH will antagonize ethanol-induced sedation identified the inferior collicular cortex as the major contributor to ethanol-induced seizures.

--Showed that multiple withdrawals from chronic ethanol treatment kindle inferior collicular seizure activity.

Current Research Projects

  • Neurobiology of Anti-Depressant Drugs
  • Molecular Basis for Ethanol-GABA Interactions
  • Molecular Basis of Ethanol Action on NMDA Receptors
  • CNS Transmitters Involved in Withdrawal-Induced Anxiety
  • Gene Therapy and Seizures