FACULTY

	Stephen Heinemann Molecular Neurobiology Laboratory Email: heinemann@salk.edu Lab Website: http://www.salk.edu/labs/mnl-h/home.html
Research Description
Stephen F. Heinemann, a professor in the Molecular Neurobiology Laboratory, studies the molecular details of communication among brain cells. The synapse plays a key role in communicating information between brain cells and it is likely that biochemical changes at the synapse underlie some aspects of higher brain function. Most plausible theories of learning and memory depend upon changes in the efficiency of chemical synapses, which probably involves changes in receptors, ion channels and neurotransmitter release. It is also now known that these molecules can be directly involved in human disease. Most drugs that are used to treat mental illness are known to work either on the receptors or the metabolism of the transmitters at the synapse. The work in the laboratory is focused on the molecular biology and physiology of the glutamate and nicotinic receptors expressed in the brain. A major goal is to understand the regulation of synaptic function and the molecular biology of learning. Among other notable achievements, his lab has isolated a gene containing the blueprints for a receptor critical to learning and memory, and identified the receptors that respond to nicotine. Since neurological ailments, such as Alzheimer’s and Parkinson’s; drug addiction; and mental disorders, such as depression and schizophrenia, are fundamentally disorders of brain cell communication, this research will provide new insights into the treatment of these disorders. Discoveries in Heinemann’s lab are currently being used by pharmaceutical and biotechnology companies to develop drugs for stroke, epilepsy, Parkinson’s and Alzheimer’s diseases, as well as mental conditions, such as nicotine addiction, depression and schizophrenia.
Recent Publications
Ballivet, M., Patrick, J., Lee, J. and Heinemann, S.: Molecular cloning of cDNA coding for the gamma subunit of the Torpedo acetylcholine receptor. Proc. Nat. Acad. Sci. 79:4466-4470. (1982) Boulter, J., Connolly, J., Deneris, E., Goldman, D., Heinemann, S., and Patrick, J.: Functional expression of two neuronal nicotinic acetylcholine receptors from cDNA clones identifies a gene family.Proc. Natl. Acad. Sci. 84:7763-7767. (1987) Goldman, D., Deneris, E., Kochhar, A., Patrick, J. and Heinemann, S.: Members of a nicotinic acetylcholine receptor gene family are expressed in different regions of the mammalian central nervous system. Cell 48:965-973 (1987) Hollmann, M., O' Shea-Greenfield, A., Rogers, S.W. and Heinemann, S.: Cloning by functional expression of a member of the glutamate receptor family. Nature 342:643-648. (1989) Elgoyhen, A.B., Johnson, D.S., Boulter, J., Vetter, D.E. and Heinemann, S.: Alpha9: An Acetylcholine Receptor with Novel Pharmacological Properties Expressed in Rat Chochlear Hair Cells, Cell 79:705-715 (1994). Vetter, D.E., Mann, J.R., Wangemann, P., Liu, Jianzhong, McLaughlin, K.J., Lesage, F., Marcus, D.C., Lazdunski, M., Heinemann, S. and Barhanin, J.: Inner Ear Defects Induced by Null Mutation of the isk Gene. Neuron 17:1251-1264 (1996). Mulle, C., Sailer, A., Pérez-Otaño, I., Dickinson-Anson, H., Castillo, P.E. Burearu, I., Maron, C., Gage, F.H., Mann, J.R., Bettler, B. and Heinemann, S.F.: Altered Synaptic Physiology and Reduced Susceptibility to Kainate-Induced Seizures in GluR6-Deficient Mice. Nature 392:61-605 (1998). Mulle, C., Sailer, A., Pérez-Otaño, I., Dickinson-Anson, H., Castillo, P.E. Burearu, I., Maron, C., Gage, F.H., Mann, J.R., Bettler, B. and Heinemann, S.F.: Altered Synaptic Physiology and Reduced Susceptibility to Kainate-Induced Seizures in GluR6-Deficient Mice. Nature 392:601-605 (1998). Vetter, D.E., Liberman, M.C., Mann, J., Barhanin, J., Boulter, J., Brown, M.C., Saffiote-Kolman, J., Heinemann, S.F. and Elgoyhen, A.B.: Role of a9 Nicotinic Ach Receptor Subunits in the Development and Function of Cochlear Efferent Innervation. Neuron 23:93-103 (1999). Contractor, A., Swanson, G.T., Sailer, A., O’Gorman, S. and Heinemann, S.F.: Identifiction of the Kainate Receptor Subunits Underlying Modulation of Excitatory Synaptic Transmission in the CA3 Region of the Hippocampus. Journal of Neuroscience, 20(22):8269-8278 (2000). Mulle, C., Sailer, A., Swanson, G.T., Brana, C., O’Gorman, S., Bettler, B. and Heinemann, S.F.: Subunit Composition of Kainate Receptors in Hippocampal Interneurons. Neuron 28:475-485 (2000). Contractor, A., Swanson, G. and Heinemann, S.F.: Kainate Receptors Are Involved in Short- and Long-Term Plasticity at Mossy Fiber Synapses in the Hippocampus. Neuron 29: 209-216 (2001). Vissel, B., Royle, G.A., Christie, B.R., Schiffer, H.H., Ghetti, A., Tritto, T., Perez-Otano, I., Radcliffe, R.A., Seamans, J., Sejnowski, T., Wehner, J.M., Collins, A.C., O’Gorman, S., and Heinemann, S.F.: The Role of RNA Editing of Kainate Receptors in Symaptic Plasticity and Seizures. Neuron 29: 217-227 (2001). Contractor, A., Swanson, G.T., Sailer, A. and Heinemann, S.F.: Kainate receptors modulate excitatory synaptic transmission in the CA3 region of the hippocampus. Neuron 29: 209-216 (2001). Contractor, A., Rogers, C., Maron, C., Henkemeyer, M., Swanson. G.T. and Heinemann, S.F.: Trans-Synaptic Eph Receptor-Ephrin Signaling in Hippocampal Mossy Fiber LTP. Scence 296: 1864-1869 (2002). Vetter, D.E., Li, C., Zhao, L., Contarion, A., Liberman, M.C., Smith, G.W., Marchuk, Y., Koob, G.F., Heinemann, S.F. Vale, W. and Lee, K.-F.: Urocortin-Deficient Mice Show Hearing Impairment and Increased Anxiety-like Behavior. Nat Genet. 2002 Aug;31(4):363-9.

Page last updated: July 14, 2009

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