Neuron tolerance during hydrocephalus

被引:23
作者
Ding, Y
McAllister, JP
Yao, B
Yan, N
Canady, AI
机构
[1] Wayne State Univ, Sch Med, Dept Neurol Surg, Detroit, MI 48201 USA
[2] Wayne State Univ, Sch Med, Dept Anat & Cell Biol, Detroit, MI 48201 USA
[3] Wayne State Univ, Sch Med, Childrens Hosp Michigan, Detroit, MI 48201 USA
关键词
neuron death; axon degeneration; ischemia; preconditioning; silver staining;
D O I
10.1016/S0306-4522(01)00166-X
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Whether or not neuron death plays a major role in pathophysiology during hydrocephalus is not well known. The goals of this study were to determine if neural degeneration occurred during hydrocephalus, and to determine if neuron tolerance developed during this pathophysiologic procedure. Neural damage as visualized by a sensitive staining technique, silver impregnation, was observed in three experimental groups: (1) adult hydrocephalic rats induced by kaolin injection into the cisterna magna, (2) adult rats with chronic hydrocephalus for 10 weeks subjected to acute forebrain ischemia induced by four-vessel occlusion, and (3) adult rats without hydrocephalus subjected to acute forebrain ischemia. The magnitude of hydrocephalus was also evaluated during this time. In mild or moderate hydrocephalus, little cell death was found. In severe hydrocephalus, axon and neuropil degeneration was extensively distributed, but cell death was still rarely observed. Although some neuron degeneration was found after acute forebrain ischemia in hydrocephalic. rats, the extensive cell death in cortical layers III and V, and in hippocampal areas CA1 and CA4 that is commonly observed in the ischemic brain without hydrocephalus, was not seen. This study suggests that neuron death was not a major pathological change in the brain during hydrocephalus, with cerebral ventricles being enlarged during the development of hydrocephalus. Less neuron death in hydrocephalic rats after acute forebrain ischemia suggests that neuronal tolerance to ischemia occurs during hydrocephalus. (C) 2001 IBRO. Published by Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:659 / 667
页数:9
相关论文
共 55 条
[1]   OVEREXPRESSION OF THE NEURAL GROWTH-ASSOCIATED PROTEIN GAP-43 INDUCES NERVE SPROUTING IN THE ADULT NERVOUS-SYSTEM OF TRANSGENIC MICE [J].
AIGNER, L ;
ARBER, S ;
KAPFHAMMER, JP ;
LAUX, T ;
SCHNEIDER, C ;
BOTTERI, F ;
BRENNER, HR ;
CARONI, P .
CELL, 1995, 83 (02) :269-278
[2]   Ischemic preconditioning and brain tolerance - Temporal histological and functional outcomes, protein synthesis requirement, and interleukin-1 receptor antagonist and early gene expression [J].
Barone, FC ;
White, RF ;
Spera, PA ;
Ellison, J ;
Currie, RW ;
Wang, XK ;
Feuerstein, GZ .
STROKE, 1998, 29 (09) :1937-1950
[3]  
BENOWITZ LI, 1991, ANN NY ACAD SCI, V627, P58
[4]  
Coggeshall RE, 1996, J COMP NEUROL, V364, P6, DOI 10.1002/(SICI)1096-9861(19960101)364:1<6::AID-CNE2>3.0.CO
[5]  
2-9
[6]  
CRAIN BJ, 1988, NEUROSCIENCE, V27, P387
[7]   REDUCED LOCAL CEREBRAL BLOOD-FLOW IN PERIVENTRICULAR WHITE-MATTER IN EXPERIMENTAL NEONATAL HYDROCEPHALUS - RESTORATION WITH CSF SHUNTING [J].
DASILVA, MC ;
MICHOWICZ, S ;
DRAKE, JM ;
CHUMAS, PD ;
TUOR, UI .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1995, 15 (06) :1057-1065
[8]   Cell death, axonal damage, and cell birth in the immature rat brain following induction of hydrocephalus [J].
Del Bigio, MR ;
Zhang, YW .
EXPERIMENTAL NEUROLOGY, 1998, 154 (01) :157-169
[9]  
DELBIGIO MR, 1999, PEDIAT NEUROSURGERY
[10]  
Du F, 1998, NEUROSCIENCE, V82, P1165