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Previous Article | Next Article
The Journal of Neuroscience, October 1, 1998, 18(19):7768-7778
Increased Neurogenesis in the Dentate Gyrus After Transient Global Ischemia in Gerbils
Jialing Liu1, Karen Solway1, Robert O. Messing2, and Frank R. Sharp1 1 Departments of Neurology and Neurosurgery, University of California at San Francisco and San Francisco Veterans Affairs Medical Center, San Francisco, California 94121, and 2 Department of Neurology, Ernest Gallo Clinic and Research Center and Graduate Programs in Neuroscience and Biomedical Sciences, University of California at San Francisco, San Francisco, California 94110
Neurogenesis in the dentate gyrus of adult rodents is regulated by NMDA receptors, adrenal steroids, environmental stimuli, and seizures. To determine whether ischemia affects neurogenesis, newly divided cells in the dentate gyrus were examined after transient global ischemia in adult gerbils. 5-Bromo-2'-deoxyuridine-5'-monophosphate (BrdU) immunohistochemistry demonstrated a 12-fold increase in cell birth in the dentate subgranular zone 1-2 weeks after 10 min bilateral common carotid artery occlusions. Two minutes of ischemia did not significantly increase BrdU incorporation. Confocal microscopy demonstrated that BrdU immunoreactive cells in the granule cell layer colocalized with neuron-specific markers for neuronal nuclear antigen, microtubule-associated protein-2, and calbindin D28k, indicating that the newly divided cells migrated from the subgranular zone into the granule cell layer and matured into neurons. Newborn cells with a neuronal phenotype were first seen 26 d after ischemia, survived for at least 7 months, were located only in the granule cell layer, and comprised ~60% of BrdU-labeled cells in the granule cell layer 6 weeks after ischemia. The increased neurogenesis was not attributable to entorhinal cortical lesions, because no cell loss was detected in this region. Ischemic preconditioning for 2 min, which protects CA1 neurons against subsequent ischemic damage, did not prevent increased neurogenesis in the granule cell layer after a subsequent severe ischemic challenge. Thus, ischemia-induced dentate neurogenesis is not attributable to CA1 neuronal loss. Enhanced neurogenesis in the dentate gyrus may be a compensatory adaptive response to ischemia-associated injury and could promote functional recovery after ischemic hippocampal injury.
Key words: neurogenesis; dentate gyrus; granule neuron; cerebral ischemia; hippocampus; CA1; NMDA receptor; entorhinal cortex; neural stem cells; BrdU; NeuN; GFAP; MAP-2; calbindin; spreading depression; subependyma; erythropoietin; FGF; BDNF
Copyright © 1998 Society for Neuroscience 0270-6474/98/18197768-11$05.00/0
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