Christopher J. McBain, Ph.D.

Photo of Dr. Chris McBain

Christopher J. McBain, Ph.D.

NICHD Senior Investigator and NINDS Adjunct Investigator
Address
SECTION ON CELLULAR & SYNAPTIC PHYSIOLOGY

BG 35 RM 3C-903
35 CONVENT DR
BETHESDA MD 20814

Dr. McBain received his BSc from the University of Aberdeen, Scotland and PhD from the University of Cambridge, England. During a postdoctoral fellowship at the University of North Carolina at Chapel Hill and Duke University, he studied glutamate receptor function, regulation of the extracellular volume fraction and hippocampal synaptic transmission. In 1993 he joined the NICHD as an Investigator within the Laboratory of Cellular and Molecular Neurophysiology. He is currently Deputy Scientific Director for Intramural Research and Chief of the Laboratory of Cellular and Synaptic Neurophysiology.

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Work in the McBain Laboratory is targeted towards understanding the development of excitatory and inhibitory synaptic transmission between specific identified neural populations within the hippocampal and cortical formations. Using electrophysiological, immunohistochemical, anatomical, molecular and genetic approaches we hope to gain significant insight into the developmental- and activity-dependent regulation of cellular and synaptic efficacy under both physiological and pathophysiological conditions.  As our model we have chosen to study subpopulations of principal and local circuit GABAergic inhibitory interneurons within the hippocampal formation. Within cortical networks the net flow of information is strongly modulated by the action of inhibitory interneurons, whose cell bodies are distributed throughout all layers of the hippocampus and comprise ~15% of the total neuronal population. Work performed in my laboratory over the last few years has contributed to a large body of literature showing that not only do the basic physiological properties of inhibitory interneurons differ from pyramidal neurons, but interneurons also possess a repertoire of both voltage gated and ligand gated channels distinct from principal neurons. These differences range from the molecular identity of receptors and channels to mechanisms of short- and long-term synaptic plasticity and signal transduction mechanisms associated with glutamate receptors. It is our hope that by understanding the basic mechanisms underlying inhibitory interneuron development and integration into their appropriate circuits we can begin to elucidate the roles played by the various neuronal and non-neuronal elements in specific clinically relevant neural circuit disorders.