Duke Institute for Brain Sciences

Research in the Liedtke-Lab is centered around TRP (transient receptor potential) ion channels. TRP channels were first reported in drosophila in 1989. A mutation in trp was the cause for the phenotype of a transient receptor potential light response. Since then, they were shown in mammals, vertebrates, invertebrates and yeast as well, not in bacteria. The fascination of 1989, namely that they play a role in sensory transduction, yet their exact role in signal transduction awaits further clarification, still holds true. Based on the discoveries of the founding members of the TRPV (TRP- vanilloid) subfamily, OSM-9 (a C. elegans TRPV channel) and TRPV1 (a mammalian TRP channel, identified as the ionotropic receptor activated by capsaicin and other vanilloids), the osmotically activated TRPV channel, TRPV4, was reported in 2000 by Liedtke et al. in a paper in Cell. In order to elucidate TRPV4's role in vivo, the gene was knocked out in mice (2003 PNAS paper by Liedtke and Friedman), and expressed as transgene in the nociceptive ASH sensory neuron in C. elegans, in the osm-9 mutant. Surprisingly, the mammalian channel directed defensive behavior in response to noxious osmotic and mechanical stimuli. Response behavior and physiology in mice is altered for the same modalities, as demonstrated by the phenotype of the Trpv4-/- mice. Trying to understand pathological pain at the transduction and transmission level, we have recently discovered a novel mechanism how chloride-extruding transporters are regulated in neurons of the central nervous system. In regards to pain transduction, we are also focusing on the interaction between innervated structures that can hurt, such as epithelia and joints, and their innervating sensory neurons in trigeminal and dorsal root ganglion. Since coming to Duke University in 2004, Dr. Liedtke has also set up a well-frequented outpatient clinic specializing in diagnosis and treatment of trigeminal pain, in particular trigeminal neuralgia and trigeminal neuropathic pain.

NC Medical Board, License to Practice Medicine, Raleigh NC, 2004

Board-certified in Neurology; German Physicians' Association, Westphalia Chapter, Muenster (Germany), 2002

Neuropathology Fellowship, Albert Einstein College of Medicine, 1994-1997

Psychiatry Residency, State Psychiatric Hospital - University of Essen-associated (Germany), 1993-1994

Neurology Residency, University Medical Center, Essen (Germany), 1991-1993

Neurology Residency, University Medical Center, Tuebingen (Germany), 1989-1991

Ph.D., University of Bochum (Germany), Medical Virology, 1990

M.D., University of Cologne (Germany), 1989

1. Yeo M, Berglund K, Augustine GJ, Liedtke W. Repression by REST-RE-1 regulates Kcc2 transcription critical for chloride-shift and GABA-switch in cortical neurons. J Neurosci 2009, 29, 14652-14662; highlighted in Faculty of 1000
2. Li J, Kanju PK, Paterson M, Cho SH, Gilmour I, Oliver T, Yasuda R, Ghio AJ, Simon SA, Liedtke W. TRPV4-mediated calcium-influx into human bronchial epithelia upon exposure to diesel exhaust particles. Environmental Health Perspectives 2011, 119, 784-793; highlighted in Faculty of 1000
3. Liedtke W, McKinley MJ, Walker L, Zhang H, Pfenning A, Drago J, Hochendoner S, Hilton D, Lawrence AJ, Denton DA. Relation of addiction genes to hypothalamic gene changes subserving genesis and gratification of a classic instinct, sodium appetite. PNAS 2011, 108, 12509-12514 (corresponding author WL; eliciting a broad media echo with reportings in the National Geographic, Sydney Morning Herald and other major newspapers, German-language high-visibility media and others; upcoming Review Article in Kidney International)