Status epilepticus-induced alterations in metabotropic glutamate receptor expression in young and adult rats

Eleonora M. Aronica, Jan A. Gorter, Marie Christine Paupard, Sonja Y. Grooms, Michael V. L. Bennett, R. Suzanne Zukin

Research output: Contribution to journalArticle

70 Citations (Scopus)

Abstract

In adult rats, kainic acid induces status epilepticus and delayed, selective cell loss of pyramidal neurons in the hippocampal CA3. In pup rats, kainate induces statue epilepticus but not the accompanying neuronal cell death. The precise mechanisms underlying this age-dependent vulnerability to seizure-induced cell death are not understood. Metabotropic glutamate receptors (mGluRs) are developmentally and spatially regulated throughout the hippocampus and are implicated in seizure-induced damage. In the present study we used in situ hybridization to examine possible changes in mGluR expression at the level of the hippocampus after status epilepticus in post- natal day 10 (P10) pup and adult (P40) rats. Status epilepticus did not alter expression of mGluR1, mGluR3, or mGluR5 mRNAs. In pup and adult rats, status epilepticus induced a reduction in expression of mGluR2 mRNA in granule cells of the dentate gyrus. This change could lead to augmented glutamate release at mossy fiber synapses on CA3 pyramidal cells and thereby promote hyperexcitation. In pup but not adult rats, mGluR4 mRNA expression was enhanced in CA3 pyramidal neurons. Upregulation of presynaptic mGluR4 in pup CA3 neurons could lead to reduced transmitter release from CA3 axons, including recurrent collaterals, thereby reducing vulnerability of neonatal CA3 neurons to seizure-induced damage. These findings indicate that status epilepticus affects mGluR expression in a gene- and cell-specific manner, and that these changes vary with the developmental stage.

Original languageEnglish (US)
Pages (from-to)8588-8595
Number of pages8
JournalJournal of Neuroscience
Volume17
Issue number21
StatePublished - 1997

Fingerprint

Metabotropic Glutamate Receptors
Status Epilepticus
Young Adult
Pyramidal Cells
Seizures
Kainic Acid
Messenger RNA
Hippocampus
Cell Death
Neurons
Dentate Gyrus
Synapses
In Situ Hybridization
Axons
Glutamic Acid
Up-Regulation
Genes

Keywords

  • Development
  • Epilepsy
  • Hippocampus
  • Metabotropic glutamate receptors
  • Receptor mRNAs
  • Seizures
  • Status epilepticus

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Status epilepticus-induced alterations in metabotropic glutamate receptor expression in young and adult rats. / Aronica, Eleonora M.; Gorter, Jan A.; Paupard, Marie Christine; Grooms, Sonja Y.; Bennett, Michael V. L.; Zukin, R. Suzanne.

In: Journal of Neuroscience, Vol. 17, No. 21, 1997, p. 8588-8595.

Research output: Contribution to journalArticle

Aronica, Eleonora M. ; Gorter, Jan A. ; Paupard, Marie Christine ; Grooms, Sonja Y. ; Bennett, Michael V. L. ; Zukin, R. Suzanne. / Status epilepticus-induced alterations in metabotropic glutamate receptor expression in young and adult rats. In: Journal of Neuroscience. 1997 ; Vol. 17, No. 21. pp. 8588-8595.
@article{0c5cf994600549e5a1c7fda670d89e19,
title = "Status epilepticus-induced alterations in metabotropic glutamate receptor expression in young and adult rats",
abstract = "In adult rats, kainic acid induces status epilepticus and delayed, selective cell loss of pyramidal neurons in the hippocampal CA3. In pup rats, kainate induces statue epilepticus but not the accompanying neuronal cell death. The precise mechanisms underlying this age-dependent vulnerability to seizure-induced cell death are not understood. Metabotropic glutamate receptors (mGluRs) are developmentally and spatially regulated throughout the hippocampus and are implicated in seizure-induced damage. In the present study we used in situ hybridization to examine possible changes in mGluR expression at the level of the hippocampus after status epilepticus in post- natal day 10 (P10) pup and adult (P40) rats. Status epilepticus did not alter expression of mGluR1, mGluR3, or mGluR5 mRNAs. In pup and adult rats, status epilepticus induced a reduction in expression of mGluR2 mRNA in granule cells of the dentate gyrus. This change could lead to augmented glutamate release at mossy fiber synapses on CA3 pyramidal cells and thereby promote hyperexcitation. In pup but not adult rats, mGluR4 mRNA expression was enhanced in CA3 pyramidal neurons. Upregulation of presynaptic mGluR4 in pup CA3 neurons could lead to reduced transmitter release from CA3 axons, including recurrent collaterals, thereby reducing vulnerability of neonatal CA3 neurons to seizure-induced damage. These findings indicate that status epilepticus affects mGluR expression in a gene- and cell-specific manner, and that these changes vary with the developmental stage.",
keywords = "Development, Epilepsy, Hippocampus, Metabotropic glutamate receptors, Receptor mRNAs, Seizures, Status epilepticus",
author = "Aronica, {Eleonora M.} and Gorter, {Jan A.} and Paupard, {Marie Christine} and Grooms, {Sonja Y.} and Bennett, {Michael V. L.} and Zukin, {R. Suzanne}",
year = "1997",
language = "English (US)",
volume = "17",
pages = "8588--8595",
journal = "Journal of Neuroscience",
issn = "0270-6474",
publisher = "Society for Neuroscience",
number = "21",

}

TY - JOUR

T1 - Status epilepticus-induced alterations in metabotropic glutamate receptor expression in young and adult rats

AU - Aronica, Eleonora M.

AU - Gorter, Jan A.

AU - Paupard, Marie Christine

AU - Grooms, Sonja Y.

AU - Bennett, Michael V. L.

AU - Zukin, R. Suzanne

PY - 1997

Y1 - 1997

N2 - In adult rats, kainic acid induces status epilepticus and delayed, selective cell loss of pyramidal neurons in the hippocampal CA3. In pup rats, kainate induces statue epilepticus but not the accompanying neuronal cell death. The precise mechanisms underlying this age-dependent vulnerability to seizure-induced cell death are not understood. Metabotropic glutamate receptors (mGluRs) are developmentally and spatially regulated throughout the hippocampus and are implicated in seizure-induced damage. In the present study we used in situ hybridization to examine possible changes in mGluR expression at the level of the hippocampus after status epilepticus in post- natal day 10 (P10) pup and adult (P40) rats. Status epilepticus did not alter expression of mGluR1, mGluR3, or mGluR5 mRNAs. In pup and adult rats, status epilepticus induced a reduction in expression of mGluR2 mRNA in granule cells of the dentate gyrus. This change could lead to augmented glutamate release at mossy fiber synapses on CA3 pyramidal cells and thereby promote hyperexcitation. In pup but not adult rats, mGluR4 mRNA expression was enhanced in CA3 pyramidal neurons. Upregulation of presynaptic mGluR4 in pup CA3 neurons could lead to reduced transmitter release from CA3 axons, including recurrent collaterals, thereby reducing vulnerability of neonatal CA3 neurons to seizure-induced damage. These findings indicate that status epilepticus affects mGluR expression in a gene- and cell-specific manner, and that these changes vary with the developmental stage.

AB - In adult rats, kainic acid induces status epilepticus and delayed, selective cell loss of pyramidal neurons in the hippocampal CA3. In pup rats, kainate induces statue epilepticus but not the accompanying neuronal cell death. The precise mechanisms underlying this age-dependent vulnerability to seizure-induced cell death are not understood. Metabotropic glutamate receptors (mGluRs) are developmentally and spatially regulated throughout the hippocampus and are implicated in seizure-induced damage. In the present study we used in situ hybridization to examine possible changes in mGluR expression at the level of the hippocampus after status epilepticus in post- natal day 10 (P10) pup and adult (P40) rats. Status epilepticus did not alter expression of mGluR1, mGluR3, or mGluR5 mRNAs. In pup and adult rats, status epilepticus induced a reduction in expression of mGluR2 mRNA in granule cells of the dentate gyrus. This change could lead to augmented glutamate release at mossy fiber synapses on CA3 pyramidal cells and thereby promote hyperexcitation. In pup but not adult rats, mGluR4 mRNA expression was enhanced in CA3 pyramidal neurons. Upregulation of presynaptic mGluR4 in pup CA3 neurons could lead to reduced transmitter release from CA3 axons, including recurrent collaterals, thereby reducing vulnerability of neonatal CA3 neurons to seizure-induced damage. These findings indicate that status epilepticus affects mGluR expression in a gene- and cell-specific manner, and that these changes vary with the developmental stage.

KW - Development

KW - Epilepsy

KW - Hippocampus

KW - Metabotropic glutamate receptors

KW - Receptor mRNAs

KW - Seizures

KW - Status epilepticus

UR - http://www.scopus.com/inward/record.url?scp=0030862387&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030862387&partnerID=8YFLogxK

M3 - Article

C2 - 9334430

AN - SCOPUS:0030862387

VL - 17

SP - 8588

EP - 8595

JO - Journal of Neuroscience

JF - Journal of Neuroscience

SN - 0270-6474

IS - 21

ER -