Progressive hippocampal loss of immunoreactive GLUT3, the neuron-specific glucose transporter, after global forebrain ischemia in the rat

A. L. McCall, M. Moholt-Siebert, A. VanBueren, N. J. Cherry, N. Lessov, N. Tiffany, M. Thompson, H. Downes, William Woodward

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Brain damage after global forebrain ischemia is worsened by prior hyperglycemia and ameliorated by antecedent hypoglycemia. To assess whether GLUT3, the neuron specific glucose transporter and its mRNA, are affected by cerebral ischemia, we investigated the hippocampal pattern of GLUT3 immunoreactivity and GLUT3 gene expression 1, 4 and 7 days after global forebrain ischemia in a rat 2-vessel occlusion model. We used a newly generated, specific, C-terminally directed polyclonal antiserum against GLUT3 to stain coronal frozen sections. Thionin staining and the microglial marker, OX42, indicated the extent of ischemic damage in hippocampus and correlated with GLUT3 loss. One day after ischemia, no significant change in hippocampal GLUT3 immunoreactivity was observed; by 4 days however, there was consistent and pronounced loss; and at 7 days the loss of GLUT3 staining was maximal. The greatest loss of GLUT3 staining was in the CA1 region, especially the strata oriens and radiatum of Ammon's horn. By contrast, GLUT3 staining was undiminished in the stratum lacunosum moleculare, in the mossy fibers of the lateral aspect of CA3 and in all but the inner-most portion of the molecular layer of the dentate gyrus, immediately adjacent to the granule cells. GLUT3 mRNA levels were not significantly altered at 24 hours and significantly declined at 4 and 7 days after ischemia in the CA1 pyramidal layer. These data are consistent with the pattern of neuronal loss and microglial activation in hippocampus. Loss of GLUT3 may affect the availability of glucose, and possibly the viability of ischemically damaged neurons.

Original languageEnglish (US)
Pages (from-to)29-38
Number of pages10
JournalBrain Research
Volume670
Issue number1
DOIs
StatePublished - Jan 23 1995

Fingerprint

Facilitative Glucose Transport Proteins
Prosencephalon
Ischemia
Staining and Labeling
Neurons
Hippocampus
Thionins
Messenger RNA
Dentate Gyrus
Frozen Sections
Brain Ischemia
Hypoglycemia
Hyperglycemia
Immune Sera
Coloring Agents
Gene Expression
Glucose
Brain

Keywords

  • Brain metabolism
  • Glucose transport
  • Neuronal protein
  • Stroke

ASJC Scopus subject areas

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

Cite this

Progressive hippocampal loss of immunoreactive GLUT3, the neuron-specific glucose transporter, after global forebrain ischemia in the rat. / McCall, A. L.; Moholt-Siebert, M.; VanBueren, A.; Cherry, N. J.; Lessov, N.; Tiffany, N.; Thompson, M.; Downes, H.; Woodward, William.

In: Brain Research, Vol. 670, No. 1, 23.01.1995, p. 29-38.

Research output: Contribution to journalArticle

McCall, AL, Moholt-Siebert, M, VanBueren, A, Cherry, NJ, Lessov, N, Tiffany, N, Thompson, M, Downes, H & Woodward, W 1995, 'Progressive hippocampal loss of immunoreactive GLUT3, the neuron-specific glucose transporter, after global forebrain ischemia in the rat', Brain Research, vol. 670, no. 1, pp. 29-38. https://doi.org/10.1016/0006-8993(94)01248-G
McCall, A. L. ; Moholt-Siebert, M. ; VanBueren, A. ; Cherry, N. J. ; Lessov, N. ; Tiffany, N. ; Thompson, M. ; Downes, H. ; Woodward, William. / Progressive hippocampal loss of immunoreactive GLUT3, the neuron-specific glucose transporter, after global forebrain ischemia in the rat. In: Brain Research. 1995 ; Vol. 670, No. 1. pp. 29-38.
@article{f1ee0628f906425c925d433b309c40bf,
title = "Progressive hippocampal loss of immunoreactive GLUT3, the neuron-specific glucose transporter, after global forebrain ischemia in the rat",
abstract = "Brain damage after global forebrain ischemia is worsened by prior hyperglycemia and ameliorated by antecedent hypoglycemia. To assess whether GLUT3, the neuron specific glucose transporter and its mRNA, are affected by cerebral ischemia, we investigated the hippocampal pattern of GLUT3 immunoreactivity and GLUT3 gene expression 1, 4 and 7 days after global forebrain ischemia in a rat 2-vessel occlusion model. We used a newly generated, specific, C-terminally directed polyclonal antiserum against GLUT3 to stain coronal frozen sections. Thionin staining and the microglial marker, OX42, indicated the extent of ischemic damage in hippocampus and correlated with GLUT3 loss. One day after ischemia, no significant change in hippocampal GLUT3 immunoreactivity was observed; by 4 days however, there was consistent and pronounced loss; and at 7 days the loss of GLUT3 staining was maximal. The greatest loss of GLUT3 staining was in the CA1 region, especially the strata oriens and radiatum of Ammon's horn. By contrast, GLUT3 staining was undiminished in the stratum lacunosum moleculare, in the mossy fibers of the lateral aspect of CA3 and in all but the inner-most portion of the molecular layer of the dentate gyrus, immediately adjacent to the granule cells. GLUT3 mRNA levels were not significantly altered at 24 hours and significantly declined at 4 and 7 days after ischemia in the CA1 pyramidal layer. These data are consistent with the pattern of neuronal loss and microglial activation in hippocampus. Loss of GLUT3 may affect the availability of glucose, and possibly the viability of ischemically damaged neurons.",
keywords = "Brain metabolism, Glucose transport, Neuronal protein, Stroke",
author = "McCall, {A. L.} and M. Moholt-Siebert and A. VanBueren and Cherry, {N. J.} and N. Lessov and N. Tiffany and M. Thompson and H. Downes and William Woodward",
year = "1995",
month = "1",
day = "23",
doi = "10.1016/0006-8993(94)01248-G",
language = "English (US)",
volume = "670",
pages = "29--38",
journal = "Brain Research",
issn = "0006-8993",
publisher = "Elsevier",
number = "1",

}

TY - JOUR

T1 - Progressive hippocampal loss of immunoreactive GLUT3, the neuron-specific glucose transporter, after global forebrain ischemia in the rat

AU - McCall, A. L.

AU - Moholt-Siebert, M.

AU - VanBueren, A.

AU - Cherry, N. J.

AU - Lessov, N.

AU - Tiffany, N.

AU - Thompson, M.

AU - Downes, H.

AU - Woodward, William

PY - 1995/1/23

Y1 - 1995/1/23

N2 - Brain damage after global forebrain ischemia is worsened by prior hyperglycemia and ameliorated by antecedent hypoglycemia. To assess whether GLUT3, the neuron specific glucose transporter and its mRNA, are affected by cerebral ischemia, we investigated the hippocampal pattern of GLUT3 immunoreactivity and GLUT3 gene expression 1, 4 and 7 days after global forebrain ischemia in a rat 2-vessel occlusion model. We used a newly generated, specific, C-terminally directed polyclonal antiserum against GLUT3 to stain coronal frozen sections. Thionin staining and the microglial marker, OX42, indicated the extent of ischemic damage in hippocampus and correlated with GLUT3 loss. One day after ischemia, no significant change in hippocampal GLUT3 immunoreactivity was observed; by 4 days however, there was consistent and pronounced loss; and at 7 days the loss of GLUT3 staining was maximal. The greatest loss of GLUT3 staining was in the CA1 region, especially the strata oriens and radiatum of Ammon's horn. By contrast, GLUT3 staining was undiminished in the stratum lacunosum moleculare, in the mossy fibers of the lateral aspect of CA3 and in all but the inner-most portion of the molecular layer of the dentate gyrus, immediately adjacent to the granule cells. GLUT3 mRNA levels were not significantly altered at 24 hours and significantly declined at 4 and 7 days after ischemia in the CA1 pyramidal layer. These data are consistent with the pattern of neuronal loss and microglial activation in hippocampus. Loss of GLUT3 may affect the availability of glucose, and possibly the viability of ischemically damaged neurons.

AB - Brain damage after global forebrain ischemia is worsened by prior hyperglycemia and ameliorated by antecedent hypoglycemia. To assess whether GLUT3, the neuron specific glucose transporter and its mRNA, are affected by cerebral ischemia, we investigated the hippocampal pattern of GLUT3 immunoreactivity and GLUT3 gene expression 1, 4 and 7 days after global forebrain ischemia in a rat 2-vessel occlusion model. We used a newly generated, specific, C-terminally directed polyclonal antiserum against GLUT3 to stain coronal frozen sections. Thionin staining and the microglial marker, OX42, indicated the extent of ischemic damage in hippocampus and correlated with GLUT3 loss. One day after ischemia, no significant change in hippocampal GLUT3 immunoreactivity was observed; by 4 days however, there was consistent and pronounced loss; and at 7 days the loss of GLUT3 staining was maximal. The greatest loss of GLUT3 staining was in the CA1 region, especially the strata oriens and radiatum of Ammon's horn. By contrast, GLUT3 staining was undiminished in the stratum lacunosum moleculare, in the mossy fibers of the lateral aspect of CA3 and in all but the inner-most portion of the molecular layer of the dentate gyrus, immediately adjacent to the granule cells. GLUT3 mRNA levels were not significantly altered at 24 hours and significantly declined at 4 and 7 days after ischemia in the CA1 pyramidal layer. These data are consistent with the pattern of neuronal loss and microglial activation in hippocampus. Loss of GLUT3 may affect the availability of glucose, and possibly the viability of ischemically damaged neurons.

KW - Brain metabolism

KW - Glucose transport

KW - Neuronal protein

KW - Stroke

UR - http://www.scopus.com/inward/record.url?scp=0028873108&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028873108&partnerID=8YFLogxK

U2 - 10.1016/0006-8993(94)01248-G

DO - 10.1016/0006-8993(94)01248-G

M3 - Article

C2 - 7719721

AN - SCOPUS:0028873108

VL - 670

SP - 29

EP - 38

JO - Brain Research

JF - Brain Research

SN - 0006-8993

IS - 1

ER -