4.8 Article

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

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NATL ACAD SCIENCES
DOI: 10.1073/pnas.1120380109

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two-photon laser scanning microscopy; ion-sensitive microelectrode

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  1. National Institutes of Health, National Institute of Neurological Disorders and Stroke [NS075177, NS078304]
  2. Keck Foundation
  3. Dana Foundation

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Recent studies have shown that cerebellar Bergmann glia display coordinated Ca2+ transients in live mice. However, the functional significance of Bergmann glial Ca2+ signaling remains poorly understood. Using transgenic mice that allow selective stimulation of glial cells, we report here that cytosolic Ca2+ 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 Ca2+ 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.

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