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

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.

SUBMITTER: Wang F

PROVIDER: S-EPMC3356677 | biostudies-literature | 2012 May

REPOSITORIES: biostudies-literature

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

Wang Fushun F Xu Qiwu Q Wang Weishan W Takano Takahiro T Nedergaard Maiken M

Proceedings of the National Academy of Sciences of the United States of America 20120430 20

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-induc ...[more]

PMID: 22547829

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