Thomas Sudhof

Honors and Awards

• Elected member, Institute of Medicine (2008)
• Elected member, National Academy of Sciences (2002)

Postdoctoral Advisees

Claudio Acuna Goycolea, Jason Aoto, Antony Boucard, Jacqueline Burre, Ozgun Gokce, Jae Won Ko, David Martinelli, Stephan Maxeiner, Sabine Mayer, Zhiping Pang, Manu Sharma, Jieun Shin, Theodoros Tsetsenis, Xiaofei Yang

Industry Relationships

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Research Interests

Human thought and perception, emotions and actions universally depend on signaling between neurons in the brain. This signalling largely happens at synapses, specialized intercellular junctions formed by pre- and postsynaptic neurons. When stimulated, a presynaptic neuron releases chemical messages—called neurotransmitters— that is recognized by a postsynaptic neuron.

For decades, the majority of neuroscientists focused their research on the postsynaptic neuron and its role in learning and memory. But throughout his career, Thomas Südhof has studied the presynaptic neuron. His collective findings have provided much of our current scientific understanding of presynaptic neuron behavior in neurotransmission and synapse formation. His work also has revealed the role of presynaptic neurons in neuropsychiatric illnesses, such as autism or neurodegenerative disorders.

Born in Germany, Südhof obtained a medical degree from the University of Gottingen in 1982. He became familiar with neuroscience when he performed research for his doctoral degree at the Max Planck Institute for Biophysical Chemistry. His thesis dealt with the release of hormones from adrenal cells, a model of neurotransmitter release.

To expand his knowledge of biochemistry and molecular biology, Südhof started to work in 1983 as a postdoctoral fellow at the laboratories of Michael Brown and Joseph Goldstein at the University of Texas Southwestern Medical Center at Dallas. He cloned the gene for the receptor of LDL (the low-density lipoprotein), a particle in the blood that transports cholesterol. Moreover, his work identified the sequences that mediate the regulation of the LDL receptor gene expression by cholesterol.

In 1986, Südhof started his own laboratory at UT Southwestern. He began his inquiry into the presynaptic neuron. At the time, what scientists mainly knew about the presynaptic neuron was that calcium ions stimulate the release of neurotransmitters from membrane-bound...

Publications

• SV2 renders primed synaptic vesicles competent for Ca2+ -induced exocytosis. Chang WP, Südhof TC. J Neurosci. 2009; 29 (4): 883-97
• Neuroligin-2 deletion selectively decreases inhibitory synaptic transmission originating from fast-spiking but not from somatostatin-positive interneurons. Gibson JR, Huber KM, Südhof TC. J Neurosci. 2009; 29 (44): 13883-97
• Conditional forebrain inactivation of nicastrin causes progressive memory impairment and age-related neurodegeneration. Tabuchi K, Chen G, Südhof TC, Shen J. J Neurosci. 2009; 29 (22): 7290-301
• Membrane fusion: grappling with SNARE and SM proteins. Südhof TC, Rothman JE. Science. 2009; 323 (5913): 474-7
• A neuroligin-4 missense mutation associated with autism impairs neuroligin-4 folding and endoplasmic reticulum export. Zhang C, Milunsky JM, Newton S, Ko J, Zhao G, Maher TA, Tager-Flusberg H, Bolliger MF, Carter AS, Boucard AA, Powell CM, Südhof TC. J Neurosci. 2009; 29 (35): 10843-54