Research in the Luscher lab revolves around understanding the structure and function of GABAergic inhibitory synapses including GABA-A receptors, receptor-associated proteins, their posttranslational modifications and how these contribute to dynamic functional modulation of synapses and neurons both under physiological conditions and in neurological and mental disorders (anxiety, depression, epilepsy).
GABA (gamma-aminobutyric acid) is the major inhibitory neurotransmitter in the brain and mediates the vast majority of neural inhibition by activation of so-called GABA-A receptors. Structurally, GABA-A receptors are heteropentameric chloride channels that include a number of different binding sites for clinically important drugs, most notably the benzodiazepines (BZs), diverse CNS-active anesthetic agents, as well as alchohol. By modulating GABA-A receptor function, these drugs can enhance or inhibit a wide variety of CNS states, including anxiety, vigilance, epileptic activity, muscle tension and memory. GABA-A receptors thereby serve as important targets for therapeutic modulation of various CNS functions. Moreover, their proper regulation is critically impotrant both during developmengt and and in the adult organism for normal brain function and mental health. Of particular interest is the role of GABA-A receptor deficits in emotional disorders (anxiety, depression), epilepsy and schizophrenia and various forms of mental retardation.