Prenatal Exposure of Rats to Ammonia Impairs NMDA Receptor Function and Affords Delayed Protection Against Ammonia Toxicity and Glutamate Neurotoxicity
| Autor: | Goizane Marcaida, Vicente Felipo, María-Dolores Miñana, Santiago Grisolia |
|---|---|
| Rok vydání: | 1995 |
| Předmět: |
Aging
medicine.medical_specialty N-Methylaspartate Normal diet Neurotoxins Glutamic Acid Biology Receptors N-Methyl-D-Aspartate Pathology and Forensic Medicine Cellular and Molecular Neuroscience Ammonia Pregnancy Cerebellum Internal medicine Lactation medicine Animals Weaning Aspartate Aminotransferases Rats Wistar Cells Cultured Neurons L-Lactate Dehydrogenase Glutamate receptor Neurotoxicity Hyperammonemia General Medicine medicine.disease Diet Rats medicine.anatomical_structure Endocrinology Neurology Prenatal Exposure Delayed Effects Toxicity NMDA receptor Female Neurology (clinical) Dizocilpine Maleate |
| Zdroj: | Europe PubMed Central |
| ISSN: | 0022-3069 |
| DOI: | 10.1097/00005072-199509000-00005 |
| Popis: | The aim of this work was to assess whether perinatal hyperammonemia impairs the function of NMDA receptors and whether this impairment affords protection against acute ammonia toxicity and glutamate and NMDA neurotoxicity. Rats were exposed to ammonia during the prenatal and lactation periods by feeding the female rats an ammonium-containing diet since day 1 of pregnancy. After weaning (at postnatal day 21), the pups were fed a normal diet with no ammonia added. This treatment resulted in a marked decrease of the growth rate of the animals, which was maintained even 1 month after normalization of ammonia levels. Rats exposed to ammonia were more resistant than controls to acute ammonia toxicity 13 days after feeding a normal diet but not at 3 months. Primary cultures of cerebellar neurons from hyperammonemic rats showed decreased binding of [3H]MK-801 and were remarkably more resistant than controls to glutamate and NMDA toxicities. Also, the increase in aspartate aminotransferase activity induced by low concentrations of NMDA was not produced in such cultures. These results indicate that exposure to ammonia during the prenatal and lactation periods results in long-lasting impairment of NMDA receptor function. This would be the reason for the delayed protection afforded by exposure to low ammonia levels against acute ammonia toxicity in animals and against glutamate and NMDA toxicity in neuronal cultures. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|