Morphology and ultrastructure of rat hippocampal formation after i.c.v. administration of N-acetyl-L-aspartyl-L-glutamate
Jazyk angličtina Země Spojené státy americké Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
14596851
DOI
10.1016/s0306-4522(03)00550-5
PII: S0306452203005505
Knihovny.cz E-zdroje
- MeSH
- agonisté excitačních aminokyselin metabolismus farmakologie MeSH
- buněčná smrt účinky léků MeSH
- časové faktory MeSH
- degenerace nervu chemicky indukované MeSH
- dipeptidy metabolismus farmakologie MeSH
- elektronová mikroskopie MeSH
- fragmentace DNA MeSH
- glutamátové receptory metabolismus MeSH
- hipokampus účinky léků patologie ultrastruktura MeSH
- injekce intraventrikulární MeSH
- koncové značení zlomů DNA in situ MeSH
- krysa rodu Rattus MeSH
- kyselina asparagová analogy a deriváty farmakologie MeSH
- kyselina glutamová farmakologie MeSH
- neurony účinky léků patologie ultrastruktura MeSH
- neuropeptidy farmakologie MeSH
- neurotoxiny metabolismus farmakologie MeSH
- počet buněk MeSH
- potkani Wistar MeSH
- receptory N-methyl-D-aspartátu agonisté metabolismus MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- agonisté excitačních aminokyselin MeSH
- dipeptidy MeSH
- glutamátové receptory MeSH
- isospaglumic acid MeSH Prohlížeč
- kyselina asparagová MeSH
- kyselina glutamová MeSH
- N-acetylaspartate MeSH Prohlížeč
- neuropeptidy MeSH
- neurotoxiny MeSH
- receptory N-methyl-D-aspartátu MeSH
N-Acetyl-L-aspartyl-L-glutamate (NAAG) is one of the most abundant neuroactive compounds in the mammalian CNS. Our recent observations have suggested that NAAG administered into rat cerebral ventricles can cause neuronal death by apparently excitotoxic mechanisms that can be antagonized by the N-methyl-D-aspartate-receptor blockers and by ligands of metabotropic glutamate receptor of Group II. Therefore, the principal aim of the present study has been to use quantitative morphology, electron microscopy and terminal deoxynucleotidyl transferase-mediated biotin dUTP nick-end labeling to study a dose- and time-dependence as well as regional distribution of neurodegeneration in hippocampi of rats after the intraventricular infusion of 0.25 micromol NAAG/ventricle and of equimolar doses of L-glutamate (L-GLU) and N-acetyl-L-aspartate (NAA), breakdown products of NAAG. The degenerative changes were observed after the infusion of 0.25 and 1.25 micromol of NAAG/ventricle, but not when a dose of 0.05 micromol of NAAG/ventricle was injected into each lateral cerebral ventricle. With a dose of 0.25 micromol of NAAG/ventricle the number of degenerated neurons reached a maximum on the fourth day after the infusion. The neuronal damage following bilateral administration of 0.25 micromol of NAAG/lateral cerebral ventricle exhibited features of a delayed neuronal degeneration, expressed mainly in the layer of dentate granule neurons. The degeneration was characterized on the basis of ultrastructural appearance and DNA-fragmentation. The morphological changes caused by L-glutamate and NAA were much smaller than those observed after the administration of NAAG and displayed a different pattern of regional distribution. The present findings suggest that NAAG can cause a loss of hippocampal neurons in vivo, apparently resulting from the neurotoxicity of NAAG itself.
Citace poskytuje Crossref.org
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