title: A concussive-like brain injury model in mice (II): selective neuronal loss in the cortex and hippocampus.
abstract: A novel concussive-like brain injury (CLBI) model characterized by transient neurobehavioral depression, short duration of brain edema, and long-lasting memory deficits has been reported in our companion paper. This was achieved by dropping a 21-g weight from a height of 25 cm onto the head of a mouse. In the present study, we examined the histopathological changes in this model. Male ddY mice were subjected to either the trauma or sham injury. Gross pathological examination of the brain 1 h posttrauma did not demonstrate subdural, subarachnoid, intraventricular, periventricular, and intraparenchymatous hemorrhage, focal lesions or contusions. Microscopic examination 24 h posttrauma with Nissl staining (cresyl violet), however, revealed a selective bilateral neuronal cell loss in the cerebral cortex and hippocampus but not in the regions of the thalamus, cerebellum, and brain stem. The characteristics of neuronal cell loss in the cortex suggested that this pathology was related in part, to the head impact dynamics, since the cell loss was noted in the central portion of the supraventricular cerebral cortex (p < 0.001), the site of the weight impact, gradually decreasing peripheral to this site, and disappearing in the areas remote from this locus. In contrast, neuronal cell loss seen in the hippocampus did not suggest that this pathology was directly associated with the impact site. Neuronal cell loss was concentrated in the pyramidal cell layer of CA2 (p < 0.01) and CA3 (p < 0.01), and a lesser degree was noted in the subfields of CA3c (p < 0.05) and the hilar region (p < 0.05) but not in the subfields of CA1 and the dentate gyrus layers. The present study characterized the histopathological change seen in the CLBI model, demonstrating the selective neuronal cell loss following weight-drop concussion in mice.
authors.affiliation: Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University School of Medicine, Japan.
authors.forename: Y P
authors.initials: YP
authors.lastname: Tang
authors.forename: Y
authors.initials: Y
authors.lastname: Noda
authors.forename: T
authors.initials: T
authors.lastname: Hasegawa
authors.forename: T
authors.initials: T
authors.lastname: Nabeshima
mesh_terms: D000818:Animals; D001924:Brain Concussion / Q000150:complications / Q000473:pathology*; D002452:Cell Count; D016923:Cell Death; D002540:Cerebral Cortex / Q000293:injuries / Q000473:pathology*; D004195:Disease Models, Animal; D006624:Hippocampus / Q000293:injuries / Q000473:pathology*; D007859:Learning Disabilities / Q000209:etiology / Q000473:pathology; D008297:Male; D008569:Memory Disorders / Q000209:etiology / Q000473:pathology; D051379:Mice; D008815:Mice, Inbred Strains; D009460:Neurologic Examination; D009474:Neurons / Q000473:pathology