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Quinolinate neurotoxicity and glutamatergic structures
G Keilhoff, G Wolf, F Stastny, W Schmidt
Jazyk angličtina Země Anglie, Velká Británie
Grantová podpora
PL143
MZ0
CEP - Centrální evidence projektů
PubMed
1970138
Knihovny.cz E-zdroje
- MeSH
- glutamáty * fyziologie MeSH
- hipokampus * patologie růst a vývoj účinky léků MeSH
- inbrední kmeny potkanů MeSH
- injekce intraventrikulární MeSH
- ketamin * farmakologie MeSH
- krysa rodu rattus MeSH
- kyselina chinolinová MeSH
- kyselina glutamová MeSH
- kyselina kynurenová farmakologie MeSH
- kyseliny chinolinové antagonisté a inhibitory toxicita MeSH
- neurotoxiny farmakologie MeSH
- pyridiny * toxicita MeSH
- věkové faktory MeSH
- vztah mezi dávkou a účinkem léčiva MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
Neurotoxic properties of quinolinic acid following intracerebroventricular application were investigated in the hippocampal formation of 12- and 30-day-old rats. Quinolinic acid neurodegenerative potency was found to depend on the survival time, the dose applied and the developmental stage of the animal. Pretreatment with kynurenic acid and ketamine as well as the transection of the perforant path were noted to protect major parts of the hippocampal cell layers from quinolinic acid-induced degenerative effects. The results are interpreted in view of a putative dependence of quinolinic acid neurotoxicity on the presence of established synaptic, in particular glutamatergic, processes which play a major role in the hippocampal formation and mature during the first postnatal weeks. For comparison, we studied local effects of quinolinic acid on superior cervical and dorsal root ganglia in which glutamate inputs obviously do not occur; no signs of neuronal vulnerability were seen.
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- $a Neurotoxic properties of quinolinic acid following intracerebroventricular application were investigated in the hippocampal formation of 12- and 30-day-old rats. Quinolinic acid neurodegenerative potency was found to depend on the survival time, the dose applied and the developmental stage of the animal. Pretreatment with kynurenic acid and ketamine as well as the transection of the perforant path were noted to protect major parts of the hippocampal cell layers from quinolinic acid-induced degenerative effects. The results are interpreted in view of a putative dependence of quinolinic acid neurotoxicity on the presence of established synaptic, in particular glutamatergic, processes which play a major role in the hippocampal formation and mature during the first postnatal weeks. For comparison, we studied local effects of quinolinic acid on superior cervical and dorsal root ganglia in which glutamate inputs obviously do not occur; no signs of neuronal vulnerability were seen.
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