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A3 - Modelling calcium-dependent signal processing in motoneurons

Bernhard Keller and Annette Zippelius

Based on the molecular, biophysical and electrophysiological research efforts of the last years, motoneurons have become a prominent model system to investigate the elementary mechanisms of cytosolic signal processing in the mammalian central nervous system. In addition, brain stem motoneurones have become the model system of choice to investigate pathophysiological disruptions of signal cascades in different forms of motoneuron disease including spinal muscular atrophy (SMA) and amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disorder. While overwhelming evidence indicates that Ca-dependent signal processing is critical for physiological and pathophysiological regulation of motoneuron function (i.e. relating synaptic inputs to appropriate firing rates), the underlying molecular and cellular mechanisms are only little understood. By using the functionally intact brain stem slice preparation from mouse, we have previously recorded and analysed on a semi-quantitative level the underlying spatio/temporal profiles of [Ca]i during physiological and pathophysiological activity (Lips & Keller 1998, Frermann et al. 1999, Vanselow & Keller 2000, Ladewig et al. 2003, Bergmann & Keller 2004). The framework of the proposed Center for Adaptive neural Systems will now permit the integration of these isolated experimental approaches into a coherent, quantitative model of Ca-dependent signal processing in specific motoneuron types.

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