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Volume 11 Issue 9, September 2005

Epilepsy is thought to be a disorder of neuronal communication. But evidence presented in this issue by Tian and colleagues (p. 973) shows that astrocytes (black cells in this image) are actively involved in the pathogenesis of seizures, releasing glutamate in a calcium-dependent manner. Original image courtesy of the authors.

Volume 11 Issue 9

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  • Neurons in the brain of individuals with focal epilepsy exhibit sustained discharges, called paroxysmal depolarization shifts. Unexpected new evidence indicates that glutamate release from glia can generate these events, and may serve to synchronize the activity of neurons (pages 973–981).

    • Michael A Rogawski
    News & Views

  • Normal cells can respond to expression of activated oncogenes by initiating cellular senescence, a permanent state of proliferative arrest. But whether this process reflects a relevant anticancer mechanism has been debated. Several studies now show that oncogene-induced senescence can occur in vivo and provides a bona fide barrier to tumorigenesis.

    • Masashi Narita
    • Scott W Lowe
    News & Views

  • Fresh approaches are needed for antiangiogenesis therapies that target blood vessel growth in tumors. Knocking down multiple regulators of angiogenesis might provide a way forward (pages 992–997).

    • Robert M Strieter
    News & Views

  • Plague bacteria are renowned for causing some of the most devastating epidemics in human history. We are now closer to understanding why: the pathogen selectively disarms key cells of the innate immune system, weakening the front-line defenses of the body.

    • Frank R DeLeo
    • B Joseph Hinnebusch
    News & Views

  • Molecules that recognize pathogens and activate the immune response are being discovered at a rapid rate. RIG-I, a new protein in this category, recognizes viral RNA. Recent studies show that RIG-I operates independently of Toll-like receptors and that it is targeted for inactivation by the hepatitis C virus.

    • Chris A Benedict
    • Carl F Ware
    News & Views
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