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Developmental changes in NMDA neurotoxicity reflect developmental changes in subunit composition of NMDA receptors

Excitotoxicity is generally studied in dissociated neurons, cultured hippocampal slices, or intact animals. However, the requirements of dissociated neurons or cultured slices to use prenatal or juvenile rats seriously limit the advantages of these systems, whereas the complexity of intact animals p... Full description

Journal Title: The Journal of neuroscience : the official journal of the Society for Neuroscience 15 March 2006, Vol.26(11), pp.2956-63
Main Author: Zhou, Miou
Other Authors: Baudry, Michel
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1529-2401 ; PMID: 16540573 Version:1
Link: http://pubmed.gov/16540573
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recordid: medline16540573
title: Developmental changes in NMDA neurotoxicity reflect developmental changes in subunit composition of NMDA receptors
format: Article
creator:
  • Zhou, Miou
  • Baudry, Michel
subjects:
  • Hippocampus -- Drug Effects
  • N-Methylaspartate -- Toxicity
  • Neurons -- Drug Effects
  • Receptors, N-Methyl-D-Aspartate -- Drug Effects
ispartof: The Journal of neuroscience : the official journal of the Society for Neuroscience, 15 March 2006, Vol.26(11), pp.2956-63
description: Excitotoxicity is generally studied in dissociated neurons, cultured hippocampal slices, or intact animals. However, the requirements of dissociated neurons or cultured slices to use prenatal or juvenile rats seriously limit the advantages of these systems, whereas the complexity of intact animals prevents detailed molecular investigations. In the present experiments, we studied developmental changes in NMDA neurotoxicity in acute hippocampal slices with lactate dehydrogenase (LDH) release in medium, propidium iodide (PI) uptake, and Nissl staining as markers of cell damage. Calpain-mediated spectrin degradation was used to test calpain involvement in NMDA neurotoxicity. NMDA treatment produced increased LDH release, PI uptake, and spectrin degradation in slices from juvenile rats but not adult rats. NMDA-induced changes in slices from young rats were blocked completely by the NMDA receptor antagonist (+)-5-methyl-10,11-dihydro-5H-dibenzo [a,d] cyclohepten-5,10-imine maleate (MK-801) and...
language: eng
source:
identifier: E-ISSN: 1529-2401 ; PMID: 16540573 Version:1
fulltext: fulltext
issn:
  • 15292401
  • 1529-2401
url: Link


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subjectHippocampus -- Drug Effects ; N-Methylaspartate -- Toxicity ; Neurons -- Drug Effects ; Receptors, N-Methyl-D-Aspartate -- Drug Effects
descriptionExcitotoxicity is generally studied in dissociated neurons, cultured hippocampal slices, or intact animals. However, the requirements of dissociated neurons or cultured slices to use prenatal or juvenile rats seriously limit the advantages of these systems, whereas the complexity of intact animals prevents detailed molecular investigations. In the present experiments, we studied developmental changes in NMDA neurotoxicity in acute hippocampal slices with lactate dehydrogenase (LDH) release in medium, propidium iodide (PI) uptake, and Nissl staining as markers of cell damage. Calpain-mediated spectrin degradation was used to test calpain involvement in NMDA neurotoxicity. NMDA treatment produced increased LDH release, PI uptake, and spectrin degradation in slices from juvenile rats but not adult rats. NMDA-induced changes in slices from young rats were blocked completely by the NMDA receptor antagonist (+)-5-methyl-10,11-dihydro-5H-dibenzo [a,d] cyclohepten-5,10-imine maleate (MK-801) and...
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abstractExcitotoxicity is generally studied in dissociated neurons, cultured hippocampal slices, or intact animals. However, the requirements of dissociated neurons or cultured slices to use prenatal or juvenile rats seriously limit the advantages of these systems, whereas the complexity of intact animals prevents detailed molecular investigations. In the present experiments, we studied developmental changes in NMDA neurotoxicity in acute hippocampal slices with lactate dehydrogenase (LDH) release in medium, propidium iodide (PI) uptake, and Nissl staining as markers of cell damage. Calpain-mediated spectrin degradation was used to test calpain involvement in NMDA neurotoxicity. NMDA treatment produced increased LDH release, PI uptake, and spectrin degradation in slices from juvenile rats but not adult rats. NMDA-induced changes in slices from young rats were blocked completely by the NMDA receptor antagonist (+)-5-methyl-10,11-dihydro-5H-dibenzo [a,d] cyclohepten-5,10-imine maleate (MK-801) and...
pmid16540573
doi10.1523/JNEUROSCI.4299-05.2006
date2006-03-15