title: Experimental epidural hematoma causes cerebral infarction and activates neocortical glial and neuronal genesis in adult guinea pigs.
abstract: Epidural hematoma (EDH) is a type of life-threatening traumatic brain injury. Little is known about the extent to which EDH may cause neural damage and regenerative response in the cerebral cortex. Here we attempted to explore these issues by using guinea pigs as an experimental model. Unilateral EDH was induced by injection of 0.1 ml autologous blood into the extradural space, with experimental effects examined at 7, 14, 30, and 60 days postlesion. An infarct developed in the cortex deep to the EDH largely after 7 days postlesion, with neuronal death occurred from layers I to V in the central infarct region, as evidenced by loss of immunoreactivity (IR) for neuron-specific nuclear antigen (NeuN). Glial fibrillary acidic protein (GFAP) IR appeared as a cellular band surrounding the infarct and extending into the periinfarct cortex along the pia. Doublecortin (DCX) IR emerged in these same areas, with labeled cells appearing as astrocytic and neuronal profiles. DCX/GFAP colocalization was found in these regions commonly at 7 and 14 days postlesion, whereas DCX/NeuN-colabeled neurons were detectable at 30 and 60 days postlesion. Subpopulations of GFAP-, DCX-, or NeuN-immunoreactive cells colocalized with the endogenous proliferative marker Ki-67 or bromodeoxyuridine (BrdU) after pulse-chase with this birth-dating marker. The results suggest that experimental EDH can cause severe neuronal loss, induce significant glial activation, and promote a certain degree of local neuronal genesis in adult guinea pig neocortex. These findings point to potential therapeutic targets for improving neuronal recovery in clinical management of EDH.
authors.affiliation: Department of Anatomy and Neurobiology, Xiangya School of Medicine, Central South University, Changsha, Hunan, China.
authors.forename: Aihua
authors.initials: A
authors.lastname: Pan
authors.forename: Ming
authors.initials: M
authors.lastname: Li
authors.forename: Jun-Yan
authors.initials: JY
authors.lastname: Gao
authors.forename: Zhi-Qin
authors.initials: ZQ
authors.lastname: Xue
authors.forename: Zhiyuan
authors.initials: Z
authors.lastname: Li
authors.forename: Xian-Yui
authors.initials: XY
authors.lastname: Yuan
authors.forename: Duan-Wu
authors.initials: DW
authors.lastname: Luo
authors.forename: Xue-Gang
authors.initials: XG
authors.lastname: Luo
authors.forename: Xiao-Xin
authors.initials: XX
authors.lastname: Yan
mesh_terms: D000818:Animals; D020520:Brain Infarction / Q000209:etiology* / Q000473:pathology; D001973:Bromodeoxyuridine / Q000378:metabolism; D002454:Cell Differentiation; D002540:Cerebral Cortex / Q000473:pathology*; D004195:Disease Models, Animal; D000089622:Doublecortin Domain Proteins; D007839:Functional Laterality; D005786:Gene Expression Regulation / Q000502:physiology; D005904:Glial Fibrillary Acidic Protein; D006168:Guinea Pigs; D006407:Hematoma, Epidural, Cranial / Q000150:complications*; D008297:Male; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D055495:Neurogenesis / Q000502:physiology*; D009457:Neuroglia / Q000473:pathology*; D009479:Neuropeptides / Q000378:metabolism; D010751:Phosphopyruvate Hydratase / Q000378:metabolism; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism
chemical_list: D000089622:Doublecortin Domain Proteins; D005904:Glial Fibrillary Acidic Protein; D008869:Microtubule-Associated Proteins; D009479:Neuropeptides; D018809:Proliferating Cell Nuclear Antigen; D010751:Phosphopyruvate Hydratase; D001973:Bromodeoxyuridine