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Welcome to

The Molecular Neuropharmacology Laboratory
at Boston University School of Medicine

Neuropharmacology Lab Group

 

Our research primarily focuses on adenosine, a naturally occurring nucleoside which exists ubiquitously throughout the body as a cellular metabolic intermediary and also functions as a neuromodulator in brain. Extracellular levels of adenosine increase drastically in response to stress insults that compromise the ATP energy metabolism. The biological functions of extracellular adenosine are mediated through four G-protein coupled receptor adenosine subtypes: A1, A2A, A2B and A3. Our long-term goal is to understand the physiological function of adenosine as a homeostatic mechanism, and its pathophysiological role as a cellular defense mechanism in response to stress insults.

Hard at Work

The brain adenosine A2A receptor is highly enriched in striatum with co-localization with D2 dopamine receptors and has been shown to antagonize the dopamine D2 receptor function is recently emerging as attractive target for treatment of Parkinsonís disease. In collaboration with our colleagues at Massachusetts General Hospital, University of Virginia and Karolinska Institute, we have developed a series of genetic knockout models with genetic deletion of adenosine A2A and A1 receptors either globally or selectively in specific brain regions (such as forebrain A2A receptor knockouts). Coupled the genetic adenosine A2A/A1 receptor knockout models with pharmacological manipulation, we aim to gain insights into the integrated, neuromodulatory function of adenosine receptors in the brain, with particular emphasis on the A2A receptor modulation of psychomotor activity and neuronal cell death in brain.

The team at a lab meeting

By studying the A2A and A1 receptor functions at behavioral, neurochemical, and cellular levels, we aim (1) to define the molecular and cellular mechanisms underlying the A2A receptor modulation of psychomotor activity in animal models of psychostimulant addiction and L-dopa-induced dyskinesia of PD and (2) to dissect out the cellular (neuronal and glial) mechanisms associated with A2A and A1 receptor modulation of brain injury in animal models of Parkinsonís disease, stroke and Huntingtonís disease.

We gratefully acknowledge the support of our research projects by the Bumpus Foundation and the Jerry McDonald Foundation for Huntingtonís Disease Research.


                      
© 2007. Molecular Neuropharmacology Lab at BU School of Medicine . All Rights Reserved.
Comments and questions to
Yu Chen.