作者: Elena V. Savvateeva-Popova , Andrey V. Popov , Thoralf Heinemannt , Peter Riederert
DOI: 10.1007/978-1-4615-0135-0_84
关键词: Glycine 、 Neuroprotection 、 Kynurenic acid 、 Cell biology 、 Mutant 、 Kynurenine pathway 、 Phenotype 、 Genetics 、 Kynurenate 、 Gene 、 Biology
摘要: A search for Drosophila mutants with phenotypes similar to human diseases might help unravel evolutionary conserved genes implicated in polygenic disorders. Among these are neurodegenerative diseases, characterized by a late onset disturbance of memory, structural brain impairments and altered content the intermediates kynurenine pathway. The ratio between kynurenate (KYNA) 3-hydroxykynurenine (3-HOK) is critical determinant neuronal viability.Therefore, cinnabar (KYNA excess) cardinal (3-HOK allow an evaluation specific roles metabolites which present physiologic concentrations mimic systemic administration. Previously we have demonstrated that mutant can serve as model dementia earliest manifestations dysfunction. Here show state control locomotor coordination parameters sound production males results from neuroprotective neurotoxic effects KYNA 3-HOK accumulated young aged mutants. high instability 1) cycle form number pulses; 2) pulse amplitude 3) rhythm courtship song alterations defective central complex demonstrate apoptosis after stress treatment. This reflect misbalance excitatory amino acids’ glycine site agonists revealed HPLC-determination. proved be normal respect studied.