Vliv vybraných farmak na předčasné degenerativní poškození mozku v experimentu. XXX XXX XXX

• MeSH
• degenerace nervu etiologie   farmakoterapie   MeSH
• modely nemocí na zvířatech MeSH

• Konspekt
• Lékařské vědy. Lékařství
• NLK Obory
• farmacie a farmakologie
• neurologie
• NLK Publikační typ
• závěrečné zprávy o řešení grantu IGA MZ ČR

• MeSH
• glutamáty metabolismus   MeSH
• krysa rodu rattus MeSH
• kyseliny chinolinové aplikace a dávkování   farmakologie   MeSH
• mozek metabolismus   účinky léků   MeSH
• novorozená zvířata MeSH
• regresní analýza MeSH
• tkáňová distribuce MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH

• MeSH
• diazooxonorleucin farmakologie   MeSH
• gama-glutamyltransferasa antagonisté a inhibitory   MeSH
• glutamáty metabolismus   MeSH
• kyselina kainová farmakologie   MeSH
• mozek metabolismus   účinky léků   MeSH
• neuroglie metabolismus   účinky léků   MeSH
• serin farmakologie   MeSH
• zvířata MeSH
• Check Tag
• zvířata MeSH

The ability of the N-methyl-D-aspartate receptor antagonists, MK-801, ketamine and alaptide [a newly synthesized cyclo(1-amino-1-cyclopentane-carbonyl-L-alanyl) with protective properties in models of hypoxia], to prevent neuronal degeneration caused by intracerebroventricular application of quinolinic acid was investigated. Neurodegenerative effects of quinolinate in the hippocampal formation were found to increase with the degree of maturity of glutamatergic target structures. A protective potency of the N-methyl-D-aspartate receptor antagonists was observed at all developmental stages studied (12- and 30-day-old and adult rats). MK-801 showed the highest efficacy, alaptide the lowest. These findings suggest a parallelism in maturity of glutamatergic transmission processes as one prerequisite of quinolinate vulnerability and postnatal increases of target fields of the protectives. Application of MK-801 or ketamine after quinolinate injection intensified their protective effects when compared to simultaneous or preadministration. This observation is interpreted as indicating that quinolinate is a prompter of a delayed neurodegenerative process rather than acting immediately as a toxicant.

• MeSH
• hipokampus * 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.

• 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