Our research of the previous years
Neuronal ion channels

The current main research focus of our team is to investigate the molecular and cellular determinants of neuronal network oscillations in cortex and hippocampus. Using appropriate conditional transgenic mouse lines in which the activity of subthreshold-activating ion channels (e.g., I(M)) can be reversibly controlled in vivo, we investigate the resulting changes at molecular, cellular, and systemic levels (e.g., KCNQ/M-channel-deficient mice; Peters et al., 2005, Nature Neuroscience).


Another focus of our research has been the investigation of the molecular mechanisms underlying disease-associated changes in cellular excitability. The question of the impact of disease-associated mutations on neuronal and cardiac ion channels, which cause the so-called ion channel diseases ("channelopathies"), has been of particular interest to us in this context. Our research approach included the cloning and characterization of novel ion channels and their subunits (Isbrandt et al., 2000, Bähring et al., 2001) and the identification and functional characterization of mutations in ion channel genes (Wedekind et al., 2004, Schulze-Bahr et al., 2003, Isbrandt et al., 2002, Schulze-Bahr et al., 2001). As a result of our studies, we identified, in collaboration with E. Schulze-Bahr, the first gene mutation in a hyperpolarization-activated pacemaker channel gene (HCN4). In addition, our investigations revealed a likely pathophysiological mechanism for disturbed rhythm generation in the sinus node (Schulze-Bahr et al., 2003), which we recently analyzed in detail by generating a conditional transgenic mouse model (Mesirca et al. 2014, Alig et al., 2009).

Consequences of creatine deficiency syndromes for brain function

Investigation of the effects of creatine synthesis deficiencies on the metabolism, cellular excitability and network activity in hippocampus and cortex and on learning and memory of knockout mice (e.g., Choe et al., 2013, Stockebrand et al., 2013, Neu et al., 2002, Schmidt et al., 2004, Chapter 74 MMBID)