Jörg von Wegerer

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Hereditary hyperekplexia is caused by disinhibition of motoneurons resulting from mutations in the ionotropic receptor for the inhibitory neurotransmitter glycine (GlyR). To study the pathomechanisms involved in vivo, we generated and analyzed transgenic mice expressing the hyperekplexia-specific dominant mutant human GlyR alpha1 subunit 271Q. Tg271Q(More)
The learning and memory of Drosophila melanogaster strains carrying the Su-var(3)6(01) mutation, which is known to affect the structural gene of a protein phosphatase 1 isoenzyme, PP1(87B), were studied in various behavioral paradigms. Three lines of Drosophila comprising the Su-var(3)6(01) mutation in different genetic backgrounds were shown to have(More)
Inhibitory glycine receptor (GlyR) and GABA(A) receptor (GABA(A)R)-mediated synaptic transmission was examined in two strains of the GlyR mutant mouse spastic and the respective wild types. The mutants display a mild and a severe neurological phenotype. Electrically evoked postsynaptic whole-cell currents were recorded from alpha-motoneurons in lumbar(More)
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