Brain glutamine synthetase increases following cerebral ischemia in the rat

Carol Petito, Marilda C. Chung, Lena M. Verkhovsky, Arthur J L Cooper

Research output: Contribution to journalArticle

117 Citations (Scopus)

Abstract

Changes in astrocyte glutamine synthetase (GS) in postischemic rat brain were evaluated and correlated with regional neuronal vulnerability or resistance to ischemia. Rats subjected to 20 or 30 min of cerebral ischemia were allowed to survive for 3 or 24 h after ischemia; normal animals served as controls. Resultant neuronal necrosis was severe in the striatum by 24 h and in the CA1 region of the hippocampus at 72 h; neurons in paramedian cortex and CA3 region of the hippocampus were not permanently damaged. Glutamine synthetase (GS) immunocytochemistry was performed on vibratome sections of paraformaldehyde-fixed brains and enzyme activity was assayed in frozen samples of cerebral cortex, striatum and hippocampus. At 3 and 24 h after ischemia, GS immunoreactivity increased and was secondary to enlargement of GS-positive cell bodies and processes as well as to increased numbers of GS-positive astrocytes. Enzyme activity also increased in cortex, striatum and hippocampus at 3 and 24 h (P ≤ 0.03). This study shows that increase in astrocyte GS occurs rapidly after ischemia, and prior studies indicate that this increase occurs in parallel with proliferative changes in astrocyte organelles. The results also suggest that astrocyte metabolism of glutamate increases after ischemia. The increased capacity for glutamine synthetase may be important in normalizing extracellular glutamate following ischemia and protecting brain from the neurotoxic effects of this excitatory amino acid.

Original languageEnglish
Pages (from-to)275-280
Number of pages6
JournalBrain Research
Volume569
Issue number2
DOIs
StatePublished - Jan 13 1992
Externally publishedYes

Fingerprint

Glutamate-Ammonia Ligase
Brain Ischemia
Astrocytes
Ischemia
Brain
Hippocampus
Glutamic Acid
Excitatory Amino Acids
Enzymes
Organelles
Cerebral Cortex
Necrosis
Immunohistochemistry
Neurons

Keywords

  • Astrocyte
  • Cerebral ischemia
  • Cortex
  • Glutamine synthetase
  • Hippocampus
  • Striatum

ASJC Scopus subject areas

  • Developmental Biology
  • Molecular Biology
  • Clinical Neurology
  • Neuroscience(all)

Cite this

Petito, C., Chung, M. C., Verkhovsky, L. M., & Cooper, A. J. L. (1992). Brain glutamine synthetase increases following cerebral ischemia in the rat. Brain Research, 569(2), 275-280. https://doi.org/10.1016/0006-8993(92)90639-Q

Brain glutamine synthetase increases following cerebral ischemia in the rat. / Petito, Carol; Chung, Marilda C.; Verkhovsky, Lena M.; Cooper, Arthur J L.

In: Brain Research, Vol. 569, No. 2, 13.01.1992, p. 275-280.

Research output: Contribution to journalArticle

Petito, C, Chung, MC, Verkhovsky, LM & Cooper, AJL 1992, 'Brain glutamine synthetase increases following cerebral ischemia in the rat', Brain Research, vol. 569, no. 2, pp. 275-280. https://doi.org/10.1016/0006-8993(92)90639-Q
Petito, Carol ; Chung, Marilda C. ; Verkhovsky, Lena M. ; Cooper, Arthur J L. / Brain glutamine synthetase increases following cerebral ischemia in the rat. In: Brain Research. 1992 ; Vol. 569, No. 2. pp. 275-280.
@article{7edd610e3a3c4a318077c17bd6ed8f18,
title = "Brain glutamine synthetase increases following cerebral ischemia in the rat",
abstract = "Changes in astrocyte glutamine synthetase (GS) in postischemic rat brain were evaluated and correlated with regional neuronal vulnerability or resistance to ischemia. Rats subjected to 20 or 30 min of cerebral ischemia were allowed to survive for 3 or 24 h after ischemia; normal animals served as controls. Resultant neuronal necrosis was severe in the striatum by 24 h and in the CA1 region of the hippocampus at 72 h; neurons in paramedian cortex and CA3 region of the hippocampus were not permanently damaged. Glutamine synthetase (GS) immunocytochemistry was performed on vibratome sections of paraformaldehyde-fixed brains and enzyme activity was assayed in frozen samples of cerebral cortex, striatum and hippocampus. At 3 and 24 h after ischemia, GS immunoreactivity increased and was secondary to enlargement of GS-positive cell bodies and processes as well as to increased numbers of GS-positive astrocytes. Enzyme activity also increased in cortex, striatum and hippocampus at 3 and 24 h (P ≤ 0.03). This study shows that increase in astrocyte GS occurs rapidly after ischemia, and prior studies indicate that this increase occurs in parallel with proliferative changes in astrocyte organelles. The results also suggest that astrocyte metabolism of glutamate increases after ischemia. The increased capacity for glutamine synthetase may be important in normalizing extracellular glutamate following ischemia and protecting brain from the neurotoxic effects of this excitatory amino acid.",
keywords = "Astrocyte, Cerebral ischemia, Cortex, Glutamine synthetase, Hippocampus, Striatum",
author = "Carol Petito and Chung, {Marilda C.} and Verkhovsky, {Lena M.} and Cooper, {Arthur J L}",
year = "1992",
month = "1",
day = "13",
doi = "10.1016/0006-8993(92)90639-Q",
language = "English",
volume = "569",
pages = "275--280",
journal = "Brain Research",
issn = "0006-8993",
publisher = "Elsevier",
number = "2",

}

TY - JOUR

T1 - Brain glutamine synthetase increases following cerebral ischemia in the rat

AU - Petito, Carol

AU - Chung, Marilda C.

AU - Verkhovsky, Lena M.

AU - Cooper, Arthur J L

PY - 1992/1/13

Y1 - 1992/1/13

N2 - Changes in astrocyte glutamine synthetase (GS) in postischemic rat brain were evaluated and correlated with regional neuronal vulnerability or resistance to ischemia. Rats subjected to 20 or 30 min of cerebral ischemia were allowed to survive for 3 or 24 h after ischemia; normal animals served as controls. Resultant neuronal necrosis was severe in the striatum by 24 h and in the CA1 region of the hippocampus at 72 h; neurons in paramedian cortex and CA3 region of the hippocampus were not permanently damaged. Glutamine synthetase (GS) immunocytochemistry was performed on vibratome sections of paraformaldehyde-fixed brains and enzyme activity was assayed in frozen samples of cerebral cortex, striatum and hippocampus. At 3 and 24 h after ischemia, GS immunoreactivity increased and was secondary to enlargement of GS-positive cell bodies and processes as well as to increased numbers of GS-positive astrocytes. Enzyme activity also increased in cortex, striatum and hippocampus at 3 and 24 h (P ≤ 0.03). This study shows that increase in astrocyte GS occurs rapidly after ischemia, and prior studies indicate that this increase occurs in parallel with proliferative changes in astrocyte organelles. The results also suggest that astrocyte metabolism of glutamate increases after ischemia. The increased capacity for glutamine synthetase may be important in normalizing extracellular glutamate following ischemia and protecting brain from the neurotoxic effects of this excitatory amino acid.

AB - Changes in astrocyte glutamine synthetase (GS) in postischemic rat brain were evaluated and correlated with regional neuronal vulnerability or resistance to ischemia. Rats subjected to 20 or 30 min of cerebral ischemia were allowed to survive for 3 or 24 h after ischemia; normal animals served as controls. Resultant neuronal necrosis was severe in the striatum by 24 h and in the CA1 region of the hippocampus at 72 h; neurons in paramedian cortex and CA3 region of the hippocampus were not permanently damaged. Glutamine synthetase (GS) immunocytochemistry was performed on vibratome sections of paraformaldehyde-fixed brains and enzyme activity was assayed in frozen samples of cerebral cortex, striatum and hippocampus. At 3 and 24 h after ischemia, GS immunoreactivity increased and was secondary to enlargement of GS-positive cell bodies and processes as well as to increased numbers of GS-positive astrocytes. Enzyme activity also increased in cortex, striatum and hippocampus at 3 and 24 h (P ≤ 0.03). This study shows that increase in astrocyte GS occurs rapidly after ischemia, and prior studies indicate that this increase occurs in parallel with proliferative changes in astrocyte organelles. The results also suggest that astrocyte metabolism of glutamate increases after ischemia. The increased capacity for glutamine synthetase may be important in normalizing extracellular glutamate following ischemia and protecting brain from the neurotoxic effects of this excitatory amino acid.

KW - Astrocyte

KW - Cerebral ischemia

KW - Cortex

KW - Glutamine synthetase

KW - Hippocampus

KW - Striatum

UR - http://www.scopus.com/inward/record.url?scp=0026598727&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026598727&partnerID=8YFLogxK

U2 - 10.1016/0006-8993(92)90639-Q

DO - 10.1016/0006-8993(92)90639-Q

M3 - Article

C2 - 1347243

AN - SCOPUS:0026598727

VL - 569

SP - 275

EP - 280

JO - Brain Research

JF - Brain Research

SN - 0006-8993

IS - 2

ER -