Astrocyte metabolism and signaling during brain ischemia

David J. Rossi, James D. Brady, Claudia Mohr

Research output: Contribution to journalReview article

375 Scopus citations

Abstract

Brain ischemia results from cardiac arrest, stroke or head trauma. These conditions can cause severe brain damage and are a leading cause of death and long-term disability. Neurons are far more susceptible to ischemic damage than neighboring astrocytes, but astrocytes have diverse and important functions in many aspects of ischemic brain damage. Here we review three main roles of astrocytes in ischemic brain damage. First, we consider astrocyte glycogen stores, which can defend the brain against hypoglycemic brain damage but may aggravate brain damage during ischemia due to enhanced lactic acidosis. Second, we review recent breakthroughs in understanding astrocytic mechanisms of transmitter release, particularly for those transmitters with known roles in ischemic brain damage: glutamate, D-serine, ATP and adenosine. Third, we discuss the role of gap-junctionally connected networks of astrocytes in mediating the spread of damaging molecules to healthy 'bystanders' during infarct expansion in stroke.

Original languageEnglish (US)
Pages (from-to)1377-1386
Number of pages10
JournalNature Neuroscience
Volume10
Issue number11
DOIs
StatePublished - Nov 1 2007

ASJC Scopus subject areas

  • Neuroscience(all)

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    Rossi, D. J., Brady, J. D., & Mohr, C. (2007). Astrocyte metabolism and signaling during brain ischemia. Nature Neuroscience, 10(11), 1377-1386. https://doi.org/10.1038/nn2004