Braissant O Honegger P Loup M Iwase K Takiguchi M Bachmann C 1999 Hyperammonemia in the brain leads to poorly understood alterations of nitric oxide (NO) synthesis. Arginine, the substrate of nitric oxide synthases, might be recycled from the citrulline produced with NO by argininosuccinate synthetase (AS) and argininosuccinate lyase (AL). The regulation of AS and AL genes during hyperammonemia is unknown in the brain. We used brain cell aggregates cultured from dissociated telencephalic cortex of rat embryos to analyze the regulation of AS and AL genes in hyperammonemia. Using RNase protection assay and non-radioactive in situ hybridization on aggregate cryosections, we show that both AS and AL genes are induced in astrocytes but not in neurons of aggregates exposed to 5 mM NH4Cl. Our work suggests that the hyperammonemic brain might increase its recycling of citrulline to arginine. application/pdf https://sonar.ch/global/documents/189459 eng info:eu-repo/semantics/altIdentifier/doi/10.1016/s0304-3940(99)00274-8 info:eu-repo/semantics/altIdentifier/pmid/10353334 info:eu-repo/semantics/openAccess Neuroscience letters. - 1999 Ammonia Animals Argininosuccinate Lyase Argininosuccinate Synthase Brain Cell Aggregation Cells, Cultured Embryonic and Fetal Development Gene Expression Regulation, Developmental Gene Expression Regulation, Enzymologic Rats Hyperammonemia: regulation of argininosuccinate synthetase and argininosuccinate lyase genes in aggregating cell cultures of fetal rat brain. http://purl.org/coar/resource_type/c_6501