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Acta Physiologica Congress

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Acta Physiologica 2012; Volume 204, Supplement 689
91st Annual Meeting of The German Physiological Society
3/22/2012-3/25/2012
Dresden, Germany


IS THE FRONTAL AND THE REAR END OF MIGRATING OLIGODENDROCYTE PROGENITORS LINKED VIA A LOCALIZED CA2+-INFLUX THROUGH MECHANO-SENSITIVE ION CHANNELS?
Abstract number: P243

Schwering1 N., Moller2 K., Dietzel2 I.D., Happel1 *P.

1Ruhr-Universitt Bochum, RUBION, Bochum, Germany
2Ruhr-Universitt Bochum, Molecular Neurobiochemistry, Bochum, Germany

Cell migration is crucial for many rearrangement processes in living organisms, ranging from development to metastases formation. Apart from the involvement of various cytoskeletal proteins essential in cell migration evidence is accumulating that a complex interplay of ion and water fluxes governs the forward motion of the nucleus. In several cell types it has been proposed that at the front of migrating cells sodium and chloride ions enter the cell, therefore increasing the osmotic pressure causing a concomitant water influx. Furthermore, it has been shown that calcium dependent potassium channels are activated at the rear end of the migrating cell. The resulting potassium outflow is most likely accompanied by an efflux of chloride, resulting in a local decrease of osmotic pressure accompanied by an efflux of water, leading to a directed movement of the cell. However, it has not been clearly resolved, how these events at the frontal and the rear end of the cell are coupled.

Using scanning ion conductance microscopy (SICM) and time-lapse Ca2+-imaging we now present evidence that prior to the acceleration of the nucleus, the frontal end of migrating oligodendrocyte precursor cells (OPCs) swells concomitant with a local intracellular Ca2+-increase, suggesting that the two spatially separated membrane processes might be linked via an influx of calcium that is triggered by a local volume increase in migrating OPCs.

To cite this abstract, please use the following information:
Acta Physiologica 2012; Volume 204, Supplement 689 :P243

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