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Proc Natl Acad Sci U S A. 2012 May 15;109(20):7911-6. doi: 10.1073/pnas.1120380109. Epub 2012 Apr 30.

Bergmann glia modulate cerebellar Purkinje cell bistability via Ca2+-dependent K+ uptake.

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1
Division of Glial Disease and Therapeutics, Center for Translational Neuromedicine, University of Rochester, Rochester, NY 14642, USA. fushun_wang@urmc.rochester.edu

Abstract

Recent studies have shown that cerebellar Bergmann glia display coordinated Ca(2+) transients in live mice. However, the functional significance of Bergmann glial Ca(2+) signaling remains poorly understood. Using transgenic mice that allow selective stimulation of glial cells, we report here that cytosolic Ca(2+) regulates uptake of K(+) by Bergmann glia, thus providing a powerful mechanism for control of Purkinje cell-membrane potential. The decline in extracellular K(+) evoked by agonist-induced Ca(2+) in Bergmann glia transiently increased spike activity of Purkinje cells in cerebellar slices as well as in live anesthetized mice. Thus, Bergmann glia play a previously unappreciated role in controlling the membrane potential and thereby the activity of adjacent Purkinje cells.

PMID:
22547829
PMCID:
PMC3356677
DOI:
10.1073/pnas.1120380109
[Indexed for MEDLINE]
Free PMC Article
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