title: Dendritic development of hippocampal CA1 pyramidal cells in a neonatal hypoxia-ischemia injury model.
abstract: It is believed that neonatal hypoxia-ischemia (HI) brain injury causes neuron loss and brain functional defects. However, the effect of HI brain injury on dendritic development of the remaining pyramidal cells of the hippocampus and the reaction of contralateral hippocampal neurons require further studies. The Morris water maze and Golgi-Cox staining were used to evaluate the learning and memory and dendritic morphology of pyramidal cells. The results of Golgi-Cox staining showed CA1 pyramidal neurons of HI injury models with fewer bifurcations and shorter dendrite length than the naive control group. The density of dendritic spines of hippocampal CA1 pyramidal neurons was significantly lower in the HI brain injury group than in controls. With respect to hippocampal function, the HI brain injury group presented cognitive deficits in the reference memory task and probe trail. In the HI group, the pyramidal cells of left hippocampus that did not experienced ischemia but did experience hypoxia had more complex dendrites and higher density of spine than the HI injury side and control. The functional implementation of injured hippocampus might depend mainly on the hypertrophy of contralateral hippocampus after HI brain injury. Corticosterone can partially prevent the hippocampal pyramidal cells from HI injury and reduce the difference of the bilateral hippocampus pyramidal cells, but there was no improvement in learning and memory.
authors.affiliation: Department of Neurobiology, College of Basic Medical Sciences, Chongqing Key Laboratory of Neurobiology, Third Military Medical University, Chongqing, China.
authors.forename: Yan Dong
authors.initials: YD
authors.lastname: Zhao
authors.forename: Shan
authors.initials: S
authors.lastname: Ou
authors.forename: Sai Yu
authors.initials: SY
authors.lastname: Cheng
authors.forename: Zhi
authors.initials: Z
authors.lastname: Xiao
authors.forename: Wen Juan
authors.initials: WJ
authors.lastname: He
authors.forename: Jin Hai
authors.initials: JH
authors.lastname: Zhang
authors.forename: Huai Zhen
authors.initials: HZ
authors.lastname: Ruan
mesh_terms: D000367:Age Factors; D000818:Animals; D000831:Animals, Newborn; D056547:CA1 Region, Hippocampal / Q000254:growth & development / Q000473:pathology*; D003345:Corticosterone / Q000494:pharmacology / Q000627:therapeutic use; D003712:Dendrites / Q000187:drug effects / Q000473:pathology* / Q000648:ultrastructure; D004195:Disease Models, Animal; D005106:Exploratory Behavior; D007839:Functional Laterality; D020925:Hypoxia-Ischemia, Brain / Q000188:drug therapy / Q000473:pathology* / Q000503:physiopathology; D018782:Maze Learning; D008568:Memory; D017966:Pyramidal Cells / Q000187:drug effects / Q000473:pathology / Q000648:ultrastructure*; D051381:Rats; D017207:Rats, Sprague-Dawley; D016622:Silver Staining; D013028:Space Perception
chemical_list: D003345:Corticosterone
keywords: Cox; Golgi; corticosterone; hippocampus; hypoxia-ischemia