OHSU
Thomas Soderling

Thomas Soderling, Ph.D.

Senior Scientist
Professor Emeritus

Email: soderlit@ohsu.edu

PubMed Listing

 

BACKGROUND

Thomas Soderling is a senior scientist in the Vollum Institute. He holds concurrent appointments as professor in the Departments of Biochemistry and Molecular Biology and Cell and Developmental Biology in the School of Medicine. After receiving his B.S. in Chemistry from the University of Idaho in 1966, Soderling pursued his Ph.D. in Biochemistry at the University of Washington and graduated in 1970. He arrived at the Vollum in 1991 after 17 years at Vanderbilt Medical School as a professor of Molecular Physiology and Biophysics and as Investigator of the Howard Hughes Medical Institute (1976-1989). At OHSU he initiated and directed (1992-1997) the Ph.D. program in neurosciences and served as associate director of the Vollum Institute (1991-2001).

 

SUMMARY OF CURRENT RESEARCH

Intracellular calcium (Ca2+) is a major regulator of cellular functions, particularly in brain cells. As the Ca2+ concentration inside the cell rises, Ca2+ interacts with calmodulin (CaM), and this complex interacts with, and alters the functions of a large number of proteins inside cells. The Soderling lab focuses on protein kinases (CaMKs) activated by binding Ca2+/CaM. These CaMKs modulate a variety of cellular functions by adding phosphate groups to proteins including ion channels, transcription factors, cytoskeletal proteins, and proteins (enzymes) that control the chemistry of the cell. The lab studies the regulatory properties of these CaMKs and their targets (substrates) in brain cells. Understanding the biology of these signaling pathways should clarify their physiological functions in cells. Studies in the lab rely on techniques of protein chemistry, molecular biology, fluorescent imaging, and electrophysiology.

Soderling and his colleagues are looking at the cellular responses regulated by these CaMKs. CaMKII, by phosphorylating glutamate receptor ion channels (AMPA receptors) and translation factors (CPEB), regulates synaptic current in learning and memory paradigms such as long-term potentiation (LTP). Recent studies have identified multiple roles for CaMKI in neuronal development and plasticity including regulation of axonal growth cone morphology, dendritic branching and maturation of spines and synapses. Thus, these CaMKs participate in distinct steps of the complex processes of neuronal development and learning/memory in the brain.

 

SELECTED PUBLICATIONS

Fortin DA, Davare MA, Srivastava T, Brady JD, Nygaard S, Derkach VA, and Soderling TR. (2010) Long-term potentiation-dependent spine enlargement requires synaptic Ca2+-permeable AMPA receptors recruited by CaM-kinase I. J. Neurosci. 30:11565-11575.

Saneyoshi T, Fortin DA, and Soderling TR. (2010) Regulation of spine and synapse formation by activity-dependent intracellular signaling pathways. Curr. Opin. Neurobiol. 20:108-115.

Davare MA, Fortin DA, Saneyoshi T, Nygaard S, Kaech S, Banker G, Soderling TR and Wayman GA. (2009) Transient receptor potential canonical 5 channels activate Ca2+/calmodulin kinase Iγ to promote axon formation in hippocampal neurons. J. Neurosci. 29:9794-9808.

Saneyoshi T, Wayman GA, Fortin D, Davare M, Hoshi N, Nozaki N, Natsume T, and Soderling TR. (2008) Activity-dependent synaptogenesis: regulation by a CaM-Kinase Kinase/CaM-Kinase I/betaPIX signaling complex. Neuron 57:94-107. (see commentary in Neuron 57:3-4)

Guire ES, Oh MC, Soderling TR and Derkach VA. (2008) Recruitment of calcium-permeable AMPA receptors during synaptic potentiation is regulated by CaM-kinase I. J. Neurosci. 28:6000-6009.

Derkach VA, Oh MC, Guire ES, and Soderling TR. (2007) Regulatory mechanisms of AMPA receptors in synaptic plasticity. Nature Rev. Neurosci. 8:101-113.

Wayman GA, Impey S, Marks D, Saneyoshi T, Grant WF, Derkach V, and Soderling TR. (2006) Activity-dependent dendritic arborization mediated by CaM-kinase I activation and enhanced CREB-dependent transcription of Wnt-2. Neuron 50:897-909. (see commentaries in Neuron 50:813-5; Science STKE 2006(342):tw220; and Nature Rev. Neurosci. 7:598.)

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