Pharmacology and Toxicology - Faculty



Kenneth M. Johnson, Ph.D.

Professor and Graduate Program Director

Affiliations

Center for Addiction Research, Department of Psychiatry and Behavioral Sciences, Graduate Program in Neuroscience

Contact Information

Phone: (409) 772-1561
Fax: (409) 772-9642
Email: kmjohnso@utmb.edu

Research Information Page

Education

B.S. 1963-1967 Stephen F. Austin University

Ph.D. 1969-1974 University of Houston

Postdoctoral Fellowship 1975-1977 Medical College of Virginia

Background

After teaching high school science for two years, I decided that I wanted to do more with my background in biology, chemistry and physics, and decided to enroll in the graduate program in Biophysical Sciences at the University of Houston. I would never have guessed that this would lead to a dissertation on the biochemical and behavioral effects of marihuana in mice and rats. Unpredictable career paths are common in science.

I was then recruited to the Medical College of Virginia (VCU) to continue this work as a postdoctoral fellow by Drs. William Dewey and Louis Harris where I learned how to use the principles of classical structure activity relationships to understand the pharmacological basis of both behavioral and biochemical effects of various cannabinoids found in marihuana, as well as some of the metabolites of marihuana found in humans. The use of basic structure activity relationships remains at the heart of my research in several areas of investigation in my lab today.

The current focus in my laboratory is on finding novel approaches for the treatment of schizophrenia. To this end, we have discovered that treatment of very young rat pups with phencyclidine (PCP, angel dust) causes symptoms later in development that mimic many of the signs of schizophrenia. Experiments using pharmacological antagonism have shown that these behavioral deficits are related to the apoptotic effects of PCP in very specific brain regions. Unlike necrosis, apoptosis is a mechanism by which cells die in a very orderly and relatively slow fashion. By using specific information about the mechanism(s) of neuronal death, we are using pharmacological approaches to disrupt this process, and then correlating these data with the behavioral effects observed. To date, we have observed that pharmacological activation of specific calcium conductance channels is able to prevent the apoptotic effects of PCP. Collaboration with chemists at the University of Illinois-Chicago and here at UTMB has led to the synthesis of new molecules that can ameliorate the neurotoxic effects of PCP. Our ultimate goal is to turn these leads into novel pharmacotherapeutic molecules for the treatment of schizophrenia.