Burt Sharp, M.D.

Burt Sharp, M.D.

Van Vleet Professor

Department of Pharmacology

Co-Director
Center for Neurobiology of Brain Disease


The University of Tennessee Health Science Center
874 Union Avenue
Memphis, TN 38163
Phone: (901) 448-6000
Fax: (901) 448-7300
Lab: 115 Crowe Research Building
Email: Burt Sharp

 

Education

  • M.D. Institution: University of Cincinnati

Links

Research Interests

This research program has dual foci involving (1) the basic neuro-chemistry and molecular neurobiology of nicotine and (2) cellular and biochemical approaches to understand the action of opioid peptides on the immune system.

The nicotine research uses in vivo microdialysis coupled with measurements of biogenic amines and excitatory amino acids to understand both the neurochemical basis for addiction to nicotine and the beneficial therapeutic effects of nicotinic agonists on hypothalamic and hippocampal function. In many of these studies, nicotine is delivered acutely through intra-jugular catheters and cannulae that are chronically implanted in specific CNS sites. Animals also learn to self-administer nicotine through operant conditioning that mimics human smoking. In vivo microdialysis in these self-administering animals permits analysis of changes in brain neurochemistry and direct correlation of these with drug-dependent behavior. Using RT-PCR, analyses are made of specific gene expression in micropunched areas of brain. Similarly, in situ hybridization analyses are used to characterize the effects of nicotine self-administration on short and longterm changes in CNS gene expression.

Dr. Sharp's research on opioid immunobiology seeks to understand the cellular and molecular basis for the modulatory effects of opiates and opioid peptides on lymphocytes, specifically T-cells. Using fluorescence flow cytometry and RT-PCR, his lab is characterizing the expression of delta opioid receptors on specific subsets of T lymphocytes. Biochemical and immunological approaches (e.g., immunoprecipitation, Western immunoblotting, receptor binding, etc.) are used to elucidate the signal transduction pathways that mediate the anti-proliferative actions of delta opioid receptors on T-cells. Their current focus is on the role of mitogen-activated protein kinases (MAPKs) in opioid signaling, as this pertains to the effects of opioids on MAPK-dependent interleukin-2 production.

Representative Publications

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