Tolerance of neonatal rat brain to acute hyperammonemia

• Published in: Brain research 2003-05, Vol.973 (1), p.31-38
• Main Authors: Garcı&#x0301, a, M.Victoria, López-Mediavilla, Casilda, Juanes de la Peña, Marı&#x0301, a C., Medina, José M.
• Format: Article
• Language: English
• Subjects: Acute Disease; Adenosine Triphosphate - metabolism; Age Factors; Ammonia - metabolism; Ammonia - toxicity; Animals; Animals, Newborn; Biological and medical sciences; Brain - drug effects; Brain - metabolism; Errors of metabolism; Female; Glutamate; Glutamic Acid - metabolism; Glutamine; Hyperammonemia; Hyperammonemia - chemically induced; Hyperammonemia - metabolism; Lactic Acid - metabolism; Male; Medical sciences; Metabolic diseases; Miscellaneous hereditary metabolic disorders; Mitochondria; Neonate; Rats; Rats, Wistar
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/S0006-8993(03)02529-0

The aim of the present work was to study the effects of hyperammonemia on brain energy metabolism in neonatal rats. Rats were rendered hyperammonemic by ammonium acetate administration. This decreased brain ATP concentrations but enhanced brain ammonia and lactate levels in both adult and neonatal rats. In adult rats, the decrease in brain ATP concentrations was accompanied by a plunge in the respiratory control rate (RCR) of brain mitochondria. However, the ammonia-induced effect on RCR was not observed in neonatal rats, suggesting that the fall in ATP levels observed in neonatal rats would not be due to an impairment of mitochondrial respiratory efficiency. However, in neonatal rats the increase in blood and brain ammonia concentrations did not change brain glutamate concentrations but decreased glutamine contents. These results may be of relevance for the understanding of the resistance of neonatal rats observed in this work to acute ammonia toxicity