Prof. Dr. Hanns Ulrich Zeilhofer

 

Main Goals, Keywords

Electrophysiological and behavioral studies on the cellular and molecular basis of pain with particular emphasis on altered neuronal communication within the spinal cord. Genetic factors predisposing for chronic pain syndromes including migraine.

Keywords: Pain, Spinal cord, Plasticity, GABA, Glycine, Migraine, Genetics

Group Members

1 professor, 2 senior scientists, 3 doctoral students, 3 technicians

Previous and Current Research

Our group focuses on the cellular and molecular basis of pain. Pain is a frequent and debilitating symptom of many diseases and causes significant socio-economical burden worldwide. Changes in the central particular spinal processing of nociceptive signals are critical to the development of chronic pathological pain.

We are particularly interested in changes in neuronal communication within the spinal cord, which underlie the generation of pain in inflammatory and neuropathic diseases. At present we focus on the contribution of inhibitory GABAergic and glycinergic neurotransmission to spinal pain control mechanisms both as a source of pain and as a potential target for novel analgesics.

Future Projects

• Evaluation of spinal inhibitory neurotransmitter receptors as potential targets for novel analgesics.
• Identification of genetic polymorphisms predisposing for exaggerated pain sensitivity.
• Generation of BAC transgenic mice expressing reporter genes (EGFP and other fluorescent proteins) in specific neuronal subpopulations and of Cre recombinase expressing mice.

Techniques and Equipment

• Electrophysiological setups for patch-clamp recordings and functional (Ca2+) imaging in spinal cord slices and primary cell cultures and cell lines
• Taqman PCR for quantification of gene expression and genotyping of SNPs
• Behavioral testing in animal models pain

Selected Publications

• Reinold H, Ahmadi S, Depner UB, Layh B, Heindl C, Hamza M, Pahl A, Brune K, Narumiya S, Müller U, Zeilhofer HU (2005): Spinal Inflammatory Hyperalgesia Is Mediated by Spinal Prostaglandin E Receptors of the EP2 Subtype. J Clin Invest 115:673–679
• Harvey RJ, Depner UB, Wässle H, Ahmadi S, Heindl C, Reinold H, Smart TG, Harvey K, Schütz B, Abo-Salem OM, Zimmer A, Poisbeau P, Welzl H, Wolfer DP, Betz H, Zeilhofer HU, Müller U (2004):GlyR 3: An essential target for spinal inflammatory pain sensitization. Science, 304, 884-887
• Ahmadi S, Muth-Selbach U, Lauterbach A, Lipfert P, Neuhuber WL, Zeilhofer HU (2003): Facilitation of spinal NMDA receptor-currents by synaptically released glycine. Science, 300, 2094-209
• Ahmadi S, Lippross S, Neuhuber WL, Zeilhofer HU (2002): PGE2 selectively blocks inhibitory glycinergic neurotransmission onto rat superficial dorsal horn neurons. Nat Neurosci 5, 34-40

Selected Lectures, Seminars or Colloquia

• Pharmakologie im Rahmen des 3. Studienjahrs für Studierende der Medizin
• Pharmakotherapie für Studierende der Medizin
• Pharmakologie und Toxikologie für Studierende der Pharmazie

Funding

Deutsche Forschungsgemeinschaft

URL

www.pharma.uzh.ch/research/neuropharmacology.html