Delayed cell death in neonatal mouse hippocampus from hypoxia-ischemia is neither apoptotic nor necrotic

被引:54
作者
Sheldon, RA
Hall, JJ
Noble, LJ
Ferriero, DM
机构
[1] Univ Calif San Francisco, Dept Neurol, Neonatal Brain Disorders Lab, San Francisco, CA 94143 USA
[2] Univ Calif San Francisco, Dept Neurosurg, San Francisco, CA 94143 USA
[3] Univ Calif San Francisco, Dept Pediat, Neonatal Brain Disorders Lab, San Francisco, CA 94143 USA
关键词
neonate; apoptosis; necrosis; injury; hippocampus; hypoxia-ischemia;
D O I
10.1016/S0304-3940(01)01788-8
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Hypoxic-ischemic (HI) injury in neonatal mice is associated with significant cell loss in hippocampus, striatum and deep layers of the cortex. The pattern of cell death in hippocampus after a moderate focal ischemic-global hypoxic insult is studied through morphologic changes in dying neurons at both the light and ultrastructural levels. Light microscopy at 24 h showed a number of injured neurons, as evidenced by dark, round, condensed nuclei, primarily in CA1 through CA3. Nuclei appeared punctate and cytoplasm vacuolated. Electron microscopy revealed that the punctate appearance of the nuclei corresponded to clumped chromatin. At 7 days after HI, injured neurons were shrunken and had a uniformly dark, angular appearance. While dying cells had an appearance consistent with apoptosis on light microscopy, cells were neither necrotic nor apoptotic at the ultrastructural level. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:165 / 168
页数:4
相关论文
共 18 条
[1]   GLUTAMATE-INDUCED NEURONAL DEATH - A SUCCESSION OF NECROSIS OR APOPTOSIS DEPENDING ON MITOCHONDRIAL-FUNCTION [J].
ANKARCRONA, M ;
DYPBUKT, JM ;
BONFOCO, E ;
ZHIVOTOVSKY, B ;
ORRENIUS, S ;
LIPTON, SA ;
NICOTERA, P .
NEURON, 1995, 15 (04) :961-973
[2]  
BEILHARZ EJ, 1995, MOL BRAIN RES, V29, P1
[3]  
CAMPAGNE MV, 1995, EUR J NEUROSCI, V7, P1627
[4]   Identification of necrotic cell death by the TUNEL assay in the hypoxic-ischemic neonatal rat brain [J].
deTorres, C ;
Munell, F ;
Ferrer, I ;
Reventos, J ;
Macaya, A .
NEUROSCIENCE LETTERS, 1997, 230 (01) :1-4
[5]   CALBINDIN-D28K IMMUNOREACTIVITY AND SELECTIVE VULNERABILITY TO ISCHEMIA IN THE DENTATE GYRUS OF THE DEVELOPING RAT [J].
GOODMAN, JH ;
WASTERLAIN, CG ;
MASSARWEH, WF ;
DEAN, E ;
SOLLAS, AL ;
SLOVITER, RS .
BRAIN RESEARCH, 1993, 606 (02) :309-314
[6]  
Han BH, 2000, NEUROBIOL DIS, V7, P38
[7]  
Ishimaru MJ, 1999, J COMP NEUROL, V408, P461
[8]   Nueurodegeneration in excitotoxicity, global cerebral ischemia, and target deprivation: A perspective on the contributions of apoptosis and necrosis [J].
Martin, LJ ;
Al-Abdulla, NA ;
Brambrink, AM ;
Kirsch, JR ;
Sieber, FE ;
Portera-Cailliau, C .
BRAIN RESEARCH BULLETIN, 1998, 46 (04) :281-309
[9]  
Nakajima W, 2000, J NEUROSCI, V20, P7994
[10]   Early neurodegeneration after hypoxia-ischemia in neonatal rat is necrosis while delayed neuronal death is apoptosis [J].
Northington, FJ ;
Ferriero, DM ;
Graham, EM ;
Traystman, RJ ;
Martin, LJ .
NEUROBIOLOGY OF DISEASE, 2001, 8 (02) :207-219