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Exp Neurobiol 2013; 22(4): 308-314
Published online December 30, 2013
© The Korean Society for Brain and Neural Sciences
Hey-Kyeong Jeong1,2, Ilo Jou1,2,3 and Eun-Hye Joe1,2,3,4*
1Department of Pharmacology, 2Neuroscience Graduate Program in Department of Biomedical Sciences, 3Chronic Inflammatory Disease Research Center, 4Brain Disease Research Center, Ajou University School of Medicine, Suwon 443-721, Korea
Correspondence to: *To whom correspondence should be addressed.
TEL: 82-31-219-5062, FAX: 82-31-219-5069
Although secondary delayed neuronal death has been considered as a therapeutic target to minimize brain damage induced by several injuries, delayed neuronal death does not occur always. In this study, we investigated possible mechanisms that prevent delayed neuronal death in the ATP-injected substantia nigra (SN) and cortex, where delayed neuronal death does not occur. In both the SN and cortex, ATP rapidly induced death of the neurons and astrocytes in the injection core area within 3 h, and the astrocytes in the penumbra region became hypertropic and rapidly surrounded the damaged areas. It was observed that the neurons survived for up to 1-3 months in the area where the astrocytes became hypertropic. The damaged areas of astrocytes gradually reduced at 3 days, 7 days, and 1-3 months. Astrocyte proliferation was detectable at 3-7 days, and vimentin was expressed in astrocytes that surrounded and/or protruded into the damaged sites. The NeuN-positive cells also reappeared in the injury sites where astrocytes reappeared. Taken together, these results suggest that astroycte survival and/or gliosis in the injured brain may be critical for neuronal survival and may prevent delayed neuronal death in the injured brain.
Keywords: brain injury, astrogliosis, delayed neuronal death