Failure of Ca2+-activated, CREB-dependent transcription in astrocytes

Authors

  • Peter D. Murray,

    1. Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland
    2. Program in Neuroscience, University of Maryland Baltimore, Baltimore, Maryland
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  • Tami J. Kingsbury,

    1. Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland
    2. Program in Neuroscience, University of Maryland Baltimore, Baltimore, Maryland
    3. Program in Oncology, University of Maryland Marlene and Stewart Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland
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  • Bruce K. Krueger

    Corresponding author
    1. Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland
    2. Program in Neuroscience, University of Maryland Baltimore, Baltimore, Maryland
    3. Department of Psychiatry, University of Maryland School of Medicine, Baltimore, Maryland
    • Department of Physiology, University of Maryland School of Medicine, 655 W. Baltimore St., Baltimore, MD 21201, USA
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Abstract

Astrocytes participate in signaling via Ca2+ transients that spread from cell to cell across a multicellular syncytium. The effect, if any, of these Ca2+ waves on the transcription of Ca2+/cAMP-regulatory element binding protein (CREB)-dependent genes is not known. We report here that, unlike neurons, increasing intracellular Ca2+ in cultured mouse cortical astrocytes failed to activate CREB-dependent transcription, even though CREB was phosphorylated at serine 133. In contrast, both CREB phosphorylation and CREB-dependent transcription were robustly stimulated by increasing cAMP. The failure of Ca2+-activated transcription in astrocytes was correlated with the absence of CaMKIV, a Ca2+-dependent protein kinase required for Ca2+-stimulated gene transcription in neurons. The inability of Ca2+ to signal via CaMKIV may insulate CREB-dependent gene transcription in astrocytes from activation by Ca2+ waves. © 2008 Wiley-Liss, Inc.

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