October 1, 1998, 18(19):7768–7778 | Jialing Liu, Karen Solway, Robert O. Messing, Frank R. Sharp
This study investigates the effect of transient global ischemia on neurogenesis in the dentate gyrus of adult gerbils. Using BrdU immunohistochemistry, the researchers found a 12-fold increase in cell birth in the dentate subgranular zone (SGZ) 1–2 weeks after 10 minutes of bilateral common carotid artery occlusion. Confocal microscopy revealed that these newly divided cells migrated from the SGZ into the granule cell layer (GCL) and matured into neurons. The newborn cells with a neuronal phenotype were first observed 26 days after ischemia and survived for at least 7 months, comprising approximately 60% of BrdU-labeled cells in the GCL 6 weeks post-ischemia. The increased neurogenesis was not attributed to entorhinal cortical lesions or ischemic preconditioning, suggesting that it is a compensatory adaptive response to ischemic injury. This finding suggests that enhanced neurogenesis in the dentate gyrus may promote functional recovery after ischemic hippocampal damage.This study investigates the effect of transient global ischemia on neurogenesis in the dentate gyrus of adult gerbils. Using BrdU immunohistochemistry, the researchers found a 12-fold increase in cell birth in the dentate subgranular zone (SGZ) 1–2 weeks after 10 minutes of bilateral common carotid artery occlusion. Confocal microscopy revealed that these newly divided cells migrated from the SGZ into the granule cell layer (GCL) and matured into neurons. The newborn cells with a neuronal phenotype were first observed 26 days after ischemia and survived for at least 7 months, comprising approximately 60% of BrdU-labeled cells in the GCL 6 weeks post-ischemia. The increased neurogenesis was not attributed to entorhinal cortical lesions or ischemic preconditioning, suggesting that it is a compensatory adaptive response to ischemic injury. This finding suggests that enhanced neurogenesis in the dentate gyrus may promote functional recovery after ischemic hippocampal damage.