Research

My diploma and MD theses in the Institute of Toxicology of the University of Tübingen under the supervision of Herbert Remmer dealt with the turnover of membrane proteins in the endoplasmic reticulum of rat liver. During a post-doctoral stay with Helmut Holzer at the Biochemistry Institute of the University of Freiburg, I worked on protein degradation and sporulation in yeast. The results provided the basis for my habilitation in biochemistry at Freiburg  University.

In 1976, I joined the lab of Jean-Pierre Changeux at the Pasteur Institute in Paris to investigate the metabolism of nicotinic acetylcholine receptors during motor endplate formation and found that the synthesis of this muscle receptor is regulated by a cyclic AMP-dependent mechanism. I then became a group leader in the Department of Neurochemistry led by Hans Thoenen at the Max Planck Institute for Psychiatry in Martinsried, where we characterized and affinity-purified the first neurotransmitter receptor from the mammalian CNS, the inhibitory glycine receptor. From 1983 to 1990, I was Associate and Full Professor at the Center for Molecular Biology of the University of Heidelberg. During this time, we identified and/or cloned different glycine and acetylcholine receptor genes and the receptor-associated protein gephyrin, which is essential for the formation of inhibitory synapses in the vertebrate nervous system.

In 1991, our group moved to Frankfurt since I had been offered the  directorship of a new department (Neurochemistry) at the Max Planck Institute for Brain Research. There, we pursued structure-function analyses of glycine receptors and glycine-binding NMDA receptors and delineated major determinants of receptor function. Using antisense approaches and gene targeting in mice, we showed that gephyrin is essential for glycine and GABAA receptor recruitment to inhibitory postsynapses. In addition, we cloned and/or functionally. characterized different pre- and postsynaptic proteins involved in neurotransmitter release, neurotransmitter re-uptake and axonal guidance. We also found that mutations in both pre- and postsynaptic components of the glycinergic inhbititory synapse cause neuromotor disease (hyperekplexia) in man and/or mouse and generated murine models of this disorder that differentially affected motor performance. At the end of 2009, the Department of Neurochemistry was closed due to my retirement. One of the former projects was continued until the end of 2012 in the Emeritus Group "Inhibitory Synapse Formation" kindly hosted by the Department of Molecular Neurobiology, Max Planck Institute for Experimental Medicine, Göttingen (Director Prof. Nils Brose).

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