Thomas S.
Reese M.D., Senior InvestigatorDr 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 StaffMilton 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 InterestsThe 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 PublicationsDegiorgis, 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 BeushausenLocalization of the linker region of Ca2+/calmodulin-dependent protein kinase II - Biophys Res Commun
263 657 1999
Contact InformationStructural 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