Apoptosis in the adult striatum after transient forebrain ischemia and the effects of ischemic severity

Yi Wen Ruan, Guang Yi Ling, Jing Lu Zhang, Zao C. Xu

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

The mechanisms of neuronal injury after cerebral ischemia have been under active investigation. The medium-size neurons in the dorsal striatum die within 24 h after transient cerebral ischemia. Using electron microscopy, the present study examined the nature of neuronal death in the striatum of adult rats following transient forebrain ischemia and tested the hypothesis that the ischemic severity might influence the nature of cell death. After severe ischemia (∼21 min ischemic depolarization), most neurons in the dorsal striatum died with swollen organelles and small irregular chromatin clumps resembling necrosis. The tissue damage in the dorsomedial striatum was less severe than that in the dorsolateral striatum and approximately 5% of the neurons in this region died with large chromatin clumps and relatively intact organelles resembling apoptosis. Some neurons displayed a mixture of necrotic- and apoptotic-like appearance. In contrast, the neurons with large somata only exhibited mild ultrastructural changes. After moderate ischemia (∼15 min ischemic depolarization), the tissue damage was less severe and the process of necrosis was temporally prolonged compared with that after severe ischemia. The apoptotic-like neuronal death was observed not only in the dorsomedial (∼6%) but also in the dorsolateral striatum (∼7%). The neurons in the striatum showed transient reversible changes after mild ischemia (∼10 min ischemic depolarization). The present study demonstrates that both apoptosis and necrosis occur in the adult striatum following transient forebrain ischemia and apoptosis occurs in the regions with less severe ischemia. These results suggest that ischemic severity might be one of the contributing factors to necrosis or apoptosis following transient global ischemia.

Original languageEnglish
Pages (from-to)228-240
Number of pages13
JournalBrain Research
Volume982
Issue number2
DOIs
StatePublished - Aug 29 2003

Fingerprint

Prosencephalon
Ischemia
Apoptosis
Neurons
Necrosis
Organelles
Chromatin
Transient Ischemic Attack
Carisoprodol
Brain Ischemia
Electron Microscopy
Cell Death
Wounds and Injuries

Keywords

  • Cell death
  • Global ischemia
  • Necrosis
  • Ultrastructure

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Apoptosis in the adult striatum after transient forebrain ischemia and the effects of ischemic severity. / Ruan, Yi Wen; Ling, Guang Yi; Zhang, Jing Lu; Xu, Zao C.

In: Brain Research, Vol. 982, No. 2, 29.08.2003, p. 228-240.

Research output: Contribution to journalArticle

Ruan, Yi Wen ; Ling, Guang Yi ; Zhang, Jing Lu ; Xu, Zao C. / Apoptosis in the adult striatum after transient forebrain ischemia and the effects of ischemic severity. In: Brain Research. 2003 ; Vol. 982, No. 2. pp. 228-240.
@article{d963916a1830487ea3b909fa51e654d7,
title = "Apoptosis in the adult striatum after transient forebrain ischemia and the effects of ischemic severity",
abstract = "The mechanisms of neuronal injury after cerebral ischemia have been under active investigation. The medium-size neurons in the dorsal striatum die within 24 h after transient cerebral ischemia. Using electron microscopy, the present study examined the nature of neuronal death in the striatum of adult rats following transient forebrain ischemia and tested the hypothesis that the ischemic severity might influence the nature of cell death. After severe ischemia (∼21 min ischemic depolarization), most neurons in the dorsal striatum died with swollen organelles and small irregular chromatin clumps resembling necrosis. The tissue damage in the dorsomedial striatum was less severe than that in the dorsolateral striatum and approximately 5{\%} of the neurons in this region died with large chromatin clumps and relatively intact organelles resembling apoptosis. Some neurons displayed a mixture of necrotic- and apoptotic-like appearance. In contrast, the neurons with large somata only exhibited mild ultrastructural changes. After moderate ischemia (∼15 min ischemic depolarization), the tissue damage was less severe and the process of necrosis was temporally prolonged compared with that after severe ischemia. The apoptotic-like neuronal death was observed not only in the dorsomedial (∼6{\%}) but also in the dorsolateral striatum (∼7{\%}). The neurons in the striatum showed transient reversible changes after mild ischemia (∼10 min ischemic depolarization). The present study demonstrates that both apoptosis and necrosis occur in the adult striatum following transient forebrain ischemia and apoptosis occurs in the regions with less severe ischemia. These results suggest that ischemic severity might be one of the contributing factors to necrosis or apoptosis following transient global ischemia.",
keywords = "Cell death, Global ischemia, Necrosis, Ultrastructure",
author = "Ruan, {Yi Wen} and Ling, {Guang Yi} and Zhang, {Jing Lu} and Xu, {Zao C.}",
year = "2003",
month = "8",
day = "29",
doi = "10.1016/S0006-8993(03)03021-X",
language = "English",
volume = "982",
pages = "228--240",
journal = "Brain Research",
issn = "0006-8993",
publisher = "Elsevier",
number = "2",

}

TY - JOUR

T1 - Apoptosis in the adult striatum after transient forebrain ischemia and the effects of ischemic severity

AU - Ruan, Yi Wen

AU - Ling, Guang Yi

AU - Zhang, Jing Lu

AU - Xu, Zao C.

PY - 2003/8/29

Y1 - 2003/8/29

N2 - The mechanisms of neuronal injury after cerebral ischemia have been under active investigation. The medium-size neurons in the dorsal striatum die within 24 h after transient cerebral ischemia. Using electron microscopy, the present study examined the nature of neuronal death in the striatum of adult rats following transient forebrain ischemia and tested the hypothesis that the ischemic severity might influence the nature of cell death. After severe ischemia (∼21 min ischemic depolarization), most neurons in the dorsal striatum died with swollen organelles and small irregular chromatin clumps resembling necrosis. The tissue damage in the dorsomedial striatum was less severe than that in the dorsolateral striatum and approximately 5% of the neurons in this region died with large chromatin clumps and relatively intact organelles resembling apoptosis. Some neurons displayed a mixture of necrotic- and apoptotic-like appearance. In contrast, the neurons with large somata only exhibited mild ultrastructural changes. After moderate ischemia (∼15 min ischemic depolarization), the tissue damage was less severe and the process of necrosis was temporally prolonged compared with that after severe ischemia. The apoptotic-like neuronal death was observed not only in the dorsomedial (∼6%) but also in the dorsolateral striatum (∼7%). The neurons in the striatum showed transient reversible changes after mild ischemia (∼10 min ischemic depolarization). The present study demonstrates that both apoptosis and necrosis occur in the adult striatum following transient forebrain ischemia and apoptosis occurs in the regions with less severe ischemia. These results suggest that ischemic severity might be one of the contributing factors to necrosis or apoptosis following transient global ischemia.

AB - The mechanisms of neuronal injury after cerebral ischemia have been under active investigation. The medium-size neurons in the dorsal striatum die within 24 h after transient cerebral ischemia. Using electron microscopy, the present study examined the nature of neuronal death in the striatum of adult rats following transient forebrain ischemia and tested the hypothesis that the ischemic severity might influence the nature of cell death. After severe ischemia (∼21 min ischemic depolarization), most neurons in the dorsal striatum died with swollen organelles and small irregular chromatin clumps resembling necrosis. The tissue damage in the dorsomedial striatum was less severe than that in the dorsolateral striatum and approximately 5% of the neurons in this region died with large chromatin clumps and relatively intact organelles resembling apoptosis. Some neurons displayed a mixture of necrotic- and apoptotic-like appearance. In contrast, the neurons with large somata only exhibited mild ultrastructural changes. After moderate ischemia (∼15 min ischemic depolarization), the tissue damage was less severe and the process of necrosis was temporally prolonged compared with that after severe ischemia. The apoptotic-like neuronal death was observed not only in the dorsomedial (∼6%) but also in the dorsolateral striatum (∼7%). The neurons in the striatum showed transient reversible changes after mild ischemia (∼10 min ischemic depolarization). The present study demonstrates that both apoptosis and necrosis occur in the adult striatum following transient forebrain ischemia and apoptosis occurs in the regions with less severe ischemia. These results suggest that ischemic severity might be one of the contributing factors to necrosis or apoptosis following transient global ischemia.

KW - Cell death

KW - Global ischemia

KW - Necrosis

KW - Ultrastructure

UR - http://www.scopus.com/inward/record.url?scp=0142070823&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0142070823&partnerID=8YFLogxK

U2 - 10.1016/S0006-8993(03)03021-X

DO - 10.1016/S0006-8993(03)03021-X

M3 - Article

C2 - 12915258

AN - SCOPUS:0142070823

VL - 982

SP - 228

EP - 240

JO - Brain Research

JF - Brain Research

SN - 0006-8993

IS - 2

ER -