Structural Cell Biology Section - Division of Intramural Research

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Thomas S. Reese Image

 Thomas S.  Reese  M.D., Senior Investigator

Dr Reese received a B.A. from Harvard College and an M.D. from Columbia College of Physicians and Surgeons. After a medical internship at Boston City Hospital he came to the NIH as a Research Associate. Except for a postdoctoral Fellowship in the Department of Anatomy at Harvard Medical School in 1965, Dr. Reese has remained at the NIH where he became a Section Chief in 1970 and a Laboratory Chief in 1983. Dr Reese was elected to the National Academy of Sciences in 1987. His research is on the basic cell biology of the neuron, particularly synapses and axonal transport.

Laboratory Staff

Milton Brightmn, Ph.D.,  , 301-496- 5091
John Chludzinski, B.S., Research Assistant , 301-435- 2805
Ayse Dosemeci, Ph.D.,  , 301-435- 2795
Linda Franklin, , Secretary , 301-496- 9951
James Galbraith, Ph.D., Postdoctoral Fellow , 301-480- 2649
Paul Gallant, Ph.D.,  , 301-435- 2707
Jennifer Petersen, B.S., Research Assistant
Ram Sihag, Ph.D., Special Expert , 301-402- 8007
Lucia Vinade, V.M.D.,  , 301-435- 2907



Research Interests

The Section on Structural Cell Biology uses advanced light and electron microscopy in conjunction with biochemistry to address important questions in cellular neurobiology. Current projects are focused on the structure and function of the post synaptic density and the molecular machinery for transporting proteins in axons. The molecular architecture of isolated PSDs is investigated by a novel immunogold/replica technique while the structural plasticity of intact PSDs is examined by thin section electron microscopy. Previous observations on post-mortem accumulation of CaM Kinase II on isolated PSDs led us to explore its accumulation in intact neurons. Sustained activation of glutamate receptors causes a reversible overall thickening and accumulation of CaMKII on PSDs. Exposure of neurons to energy-depleting conditions and excitotoxic stress promote similar changes, but now CaMKII also appears in discrete clusters throughout the cell. These clusters have been isolated and shown to be essentially composed of CaMKII. We are, thus, uncovering (with A. Dosemeci at MBL, Woods Hole) a mechanism that could protect the neuron during excessive activity by decommissioning CaMKII while maintaining calmodulin trapping. The conditions for and function of accumulation of CaMKII at PSDs are under investigation.

Selected Recent Publications

Degiorgis, J., Reese, T., Bearer, E.,
Assocoaton of nonmuscle myosin II with axoplasmic organelles - Mo;l Biol Cell  13 1046-1057 2002

Ayse Dosemeci, T S Reese, J D Petersen and Jung-Hwa Tao-Cheng
A novel particulate form of Ca2+/calmodulin-dependent protein kinase II in neurons.  - J. Neuroscience  20(9) 3076-84 2000

E.L. Bearer and T.S. Reese.
Association of Actin Filaments with Axonal Microtubule Tracts - J Neurocytology   28 85 1999

Galbraith, J. A., Reese, T.S., Schlief, M.L. & Gallant, P.E.
Slow transport of unpolymerized tubulin and polymerized neurofilament in the squid giant axon - Proc. Natl. Acad. Sci.   96 11589 1999

Ayse Dosemeci, T. S. Reese, J. D. Petersen, Calvin Choi and Sven Beushausen
Localization of the linker region of Ca2+/calmodulin-dependent protein kinase II - Biophys Res Commun   263 657 1999



Contact Information

Structural Cell Biology Section Laboratory of Neurobiology, NINDS  Building 49, Room 3E13  49 Convent Drive, MSC 4477 Bethesda MD  20892-4477

Telephone: 301-496- 1354 (office), 301- 496-1296 (laboratory), 301-480- 1485 (fax), Email: reeset@mail.nih.gov