Abstract
The delayed neuronal death (DND) resulting from brief forebrain ischemia has recently been reported to be markedly attenuated by parenteral administration of the reversible protein synthesis inhibitor, anisomycin. Previous work suggests that ischemia-induced DND is mediated by glutamate acting at one or more glutamate receptors, since glutamate receptor antagonists have been reported to reduce ischemia-induced DND. Consequently, we tested whether anisomycin could modify DND induced by direct intracerebral administration of the excitotoxins, N-methyl-d-aspartate (NMDA), α-amino-3-hydroxy-5-methylisoxasole (AMPA) or kainic acid. Anisomycin, administered parenterally, in multiple doses did not alter DND induced by any of these excitotoxins, not did combined parenteral and direct intracerebral injection of anisomycin protect against DND induced by AMPA. Thus, neurotoxicity induced by direct intracerebral administration of NMDA, AMPA or kainic acid does not appear to require de novo protein synthesis, and, therefore is not likely to be mediated by the expression of a programmed cell death cascade.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 168-170 |
| Number of pages | 3 |
| Journal | Brain Research |
| Volume | 581 |
| Issue number | 1 |
| DOIs | |
| State | Published - May 22 1992 |
| Externally published | Yes |
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Keywords
- Excitotoxicity
- Glutamate receptor
- Protein synthesis inhibitor
ASJC Scopus subject areas
- Developmental Biology
- Molecular Biology
- Clinical Neurology
- Neuroscience(all)
Cite this
Failure of a protein synthesis inhibitor to modify glutamate receptor-mediated neurotoxicity in vivo. / Leppin, C.; Finiels-Marlier, F.; Crawley, Jacqueline; Montpied, P.; Paul, S. M.
In: Brain Research, Vol. 581, No. 1, 22.05.1992, p. 168-170.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Failure of a protein synthesis inhibitor to modify glutamate receptor-mediated neurotoxicity in vivo
AU - Leppin, C.
AU - Finiels-Marlier, F.
AU - Crawley, Jacqueline
AU - Montpied, P.
AU - Paul, S. M.
PY - 1992/5/22
Y1 - 1992/5/22
N2 - The delayed neuronal death (DND) resulting from brief forebrain ischemia has recently been reported to be markedly attenuated by parenteral administration of the reversible protein synthesis inhibitor, anisomycin. Previous work suggests that ischemia-induced DND is mediated by glutamate acting at one or more glutamate receptors, since glutamate receptor antagonists have been reported to reduce ischemia-induced DND. Consequently, we tested whether anisomycin could modify DND induced by direct intracerebral administration of the excitotoxins, N-methyl-d-aspartate (NMDA), α-amino-3-hydroxy-5-methylisoxasole (AMPA) or kainic acid. Anisomycin, administered parenterally, in multiple doses did not alter DND induced by any of these excitotoxins, not did combined parenteral and direct intracerebral injection of anisomycin protect against DND induced by AMPA. Thus, neurotoxicity induced by direct intracerebral administration of NMDA, AMPA or kainic acid does not appear to require de novo protein synthesis, and, therefore is not likely to be mediated by the expression of a programmed cell death cascade.
AB - The delayed neuronal death (DND) resulting from brief forebrain ischemia has recently been reported to be markedly attenuated by parenteral administration of the reversible protein synthesis inhibitor, anisomycin. Previous work suggests that ischemia-induced DND is mediated by glutamate acting at one or more glutamate receptors, since glutamate receptor antagonists have been reported to reduce ischemia-induced DND. Consequently, we tested whether anisomycin could modify DND induced by direct intracerebral administration of the excitotoxins, N-methyl-d-aspartate (NMDA), α-amino-3-hydroxy-5-methylisoxasole (AMPA) or kainic acid. Anisomycin, administered parenterally, in multiple doses did not alter DND induced by any of these excitotoxins, not did combined parenteral and direct intracerebral injection of anisomycin protect against DND induced by AMPA. Thus, neurotoxicity induced by direct intracerebral administration of NMDA, AMPA or kainic acid does not appear to require de novo protein synthesis, and, therefore is not likely to be mediated by the expression of a programmed cell death cascade.
KW - Excitotoxicity
KW - Glutamate receptor
KW - Protein synthesis inhibitor
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UR - http://www.scopus.com/inward/citedby.url?scp=0026654647&partnerID=8YFLogxK
U2 - 10.1016/0006-8993(92)90359-H
DO - 10.1016/0006-8993(92)90359-H
M3 - Article
C2 - 1379868
AN - SCOPUS:0026654647
VL - 581
SP - 168
EP - 170
JO - Brain Research
JF - Brain Research
SN - 0006-8993
IS - 1
ER -