Pradeep G. Bhide, Ph.D.
Neuroscience Center at Massachusetts General Hospital

Massachusetts General Hospital – East
Building 149
13th Street
Charlestown, MA 02129

Telephone: 617-726-5763
E-mail: bhide@helix.mgh.harvard.edu

Biography
Dr. Bhide received a degree in Veterinary Medicine from Bangalore, India and a PhD in Neuroscience from the University of Aberdeen, Scotland. He received postdoctoral training in developmental neurobiology at University College London, England and Yale University, New Haven, CT.

Research Program
The research focus of our laboratory is on brain development, especially on the role of dopamine in fundamental aspects of morphogenesis, including neurogenesis, neuronal migration, process elongation, synapse formation and synaptic plasticity. Dopamine is a major constituent of the neurochemical environment of the developing and mature brain.

Our laboratory has discovered a novel role for dopamine in brain development by showing that dopamine receptor activation modulates neurogenesis in the embryonic mouse brain. The two major types of dopamine receptors, namely D1- and D2-like receptors produce opposite effects on the cell cycle, the molecular engine that drives neurogenesis. Activation of the D1-like receptors promotes cell cycle exit, whereas activation of the D2-like receptors promotes cell cycle re-entry and suppresses cell cycle exit. The D1-like receptors predominate over the D2-like receptors in the embryonic brain. Therefore, dopamine's effects on neurogenesis in the embryonic forebrain are D1-like effects.

Our current efforts are directed toward examining the role of dopamine receptor activation in neuronal migration, differentiation and survival in the embryonic brain, as well as fundamental perturbations in this process following cocaine exposure in utero and in dystonia. Our laboratory is also developing a transgenic mouse model in which dopamine receptor genes are overexpressed selectively in the CNS neuroepithelium (under the control of the nestin promoter) or postmitotic neurons (under the control of neuron specific enolase promoter) and electively, at specific periods of brain development (under the control of a tetracycline regulated promoter). This mouse model is expected to help elucidate the long-term effects of transient imbalance in dopamine signaling on neuronal and glial cell development.

Our laboratory also uses an in vitro slice method to study the effects of dopamine receptor activation on neuronal migration from the basal forebrain to the cerebral wall in the embryonic mouse brain. In addition some of the ongoing work involves delivery of dopamine receptor transgenes to the embryonic brain by using in utero electroporation.

Publications
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• Ohtani N, Goto T, Waeber C, Bhide PG. Dopamine modulates cell cycle in the lateral ganglionic eminence. J Neurosci. 2003; 23(7): 2840-50.
  
• Crandall JE, Hackett HE, Tobet SA, Kosofsky BE, Bhide PG. Cocaine exposure decreases GABA neuron migration from the ganglionic eminence to the cerebral cortex in embryonic mice. Cerebral Cortex 2004; 14:665-675.
  
• Popolo M, McCarthy DM, Bhide PG. Dopamine modulates precursor cell proliferation and differentiation in the embryonic mouse telencephalon. Developmental Neuroscience 2004; In Press.