Abstract
Global cerebral ischemia selectively damages neurons, but its contribution to glial cell death is uncertain. Accordingly, adult male rats were sacrificed by perfusion fixation at 1, 2, 3, 5, and 14 days following 10 minutes of global ischemia. This insult produces CA1 hippocampal neuronal death at post-ischemic (PI) day 3, but minor or no damage to neurons in other regions. In situ end labeling (ISEL) and immunohistochemistry identified fragmented DNA of dead or dying gila and distinguished glial subtypes. Rare ISEL-positive oligodendroglia, astrocytes, and microglia were present in control brain. Apoptotic bodies and ISEL-positive gila significantly increased at PI day 1 in cortex and thalamus (p < 0.05), but were similar to controls in other regions and at other PI intervals. Most were oligodendroglia, although ISEL-positive microglia and astrocytes were also observed. These results show that oligodendroglia die rapidly after brief global ischemia and are more sensitive than neurons in certain brain regions. Their selective vulnerability to ischemia may be responsible for the delayed white matter damage following anoxia or CO poisoning or that associated with white matter arteriopathies. Glial apoptosis could contribute to the DNA ladders of apoptotic oligonucleosomes that have been found in post-ischemic brain.
| Original language | English |
|---|---|
| Pages (from-to) | 231-238 |
| Number of pages | 8 |
| Journal | Journal of Neuropathology and Experimental Neurology |
| Volume | 57 |
| Issue number | 3 |
| State | Published - Mar 1 1998 |
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Keywords
- Apoptosis
- Glia
- Ischemia
- Necrosis
- Oligodendroglia
- Rat brain
ASJC Scopus subject areas
- Pathology and Forensic Medicine
- Neuroscience(all)
Cite this
Selective glial vulnerability following transient global ischemia in rat brain. / Petito, Carol; Olarte, John Paul; Roberts, Brenda; Nowak, Thaddeus S.; Pulsinelli, William A.
In: Journal of Neuropathology and Experimental Neurology, Vol. 57, No. 3, 01.03.1998, p. 231-238.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Selective glial vulnerability following transient global ischemia in rat brain
AU - Petito, Carol
AU - Olarte, John Paul
AU - Roberts, Brenda
AU - Nowak, Thaddeus S.
AU - Pulsinelli, William A.
PY - 1998/3/1
Y1 - 1998/3/1
N2 - Global cerebral ischemia selectively damages neurons, but its contribution to glial cell death is uncertain. Accordingly, adult male rats were sacrificed by perfusion fixation at 1, 2, 3, 5, and 14 days following 10 minutes of global ischemia. This insult produces CA1 hippocampal neuronal death at post-ischemic (PI) day 3, but minor or no damage to neurons in other regions. In situ end labeling (ISEL) and immunohistochemistry identified fragmented DNA of dead or dying gila and distinguished glial subtypes. Rare ISEL-positive oligodendroglia, astrocytes, and microglia were present in control brain. Apoptotic bodies and ISEL-positive gila significantly increased at PI day 1 in cortex and thalamus (p < 0.05), but were similar to controls in other regions and at other PI intervals. Most were oligodendroglia, although ISEL-positive microglia and astrocytes were also observed. These results show that oligodendroglia die rapidly after brief global ischemia and are more sensitive than neurons in certain brain regions. Their selective vulnerability to ischemia may be responsible for the delayed white matter damage following anoxia or CO poisoning or that associated with white matter arteriopathies. Glial apoptosis could contribute to the DNA ladders of apoptotic oligonucleosomes that have been found in post-ischemic brain.
AB - Global cerebral ischemia selectively damages neurons, but its contribution to glial cell death is uncertain. Accordingly, adult male rats were sacrificed by perfusion fixation at 1, 2, 3, 5, and 14 days following 10 minutes of global ischemia. This insult produces CA1 hippocampal neuronal death at post-ischemic (PI) day 3, but minor or no damage to neurons in other regions. In situ end labeling (ISEL) and immunohistochemistry identified fragmented DNA of dead or dying gila and distinguished glial subtypes. Rare ISEL-positive oligodendroglia, astrocytes, and microglia were present in control brain. Apoptotic bodies and ISEL-positive gila significantly increased at PI day 1 in cortex and thalamus (p < 0.05), but were similar to controls in other regions and at other PI intervals. Most were oligodendroglia, although ISEL-positive microglia and astrocytes were also observed. These results show that oligodendroglia die rapidly after brief global ischemia and are more sensitive than neurons in certain brain regions. Their selective vulnerability to ischemia may be responsible for the delayed white matter damage following anoxia or CO poisoning or that associated with white matter arteriopathies. Glial apoptosis could contribute to the DNA ladders of apoptotic oligonucleosomes that have been found in post-ischemic brain.
KW - Apoptosis
KW - Glia
KW - Ischemia
KW - Necrosis
KW - Oligodendroglia
KW - Rat brain
UR - http://www.scopus.com/inward/record.url?scp=0031917722&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0031917722&partnerID=8YFLogxK
M3 - Article
C2 - 9600215
AN - SCOPUS:0031917722
VL - 57
SP - 231
EP - 238
JO - American Journal of Psychotherapy
JF - American Journal of Psychotherapy
SN - 0002-9564
IS - 3
ER -