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Reduced Serotonin and 3‐Hydroxyanthranilic Acid Levels in Serum of Cystatin B‐Deficient Mice, a Model System for Progressive Myoclonus Epilepsy
Author(s) -
Arbatova Jelena,
D'Amato Elena,
Vaarmann Annika,
Zharkovsky Alex,
Reeben Mati
Publication year - 2005
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1167.2005.01008.x
Subject(s) - kynurenine , tryptophan , metabolite , serotonin , endocrinology , medicine , kynurenine pathway , biology , cystatin c , progressive myoclonus epilepsy , epilepsy , biochemistry , amino acid , creatinine , receptor , neuroscience
Summary: Purpose: To evaluate the levels of tryptophan and its metabolites along serotonin (5‐HT) and kynurenine (KYN) pathways in serum of progressive myoclonus epilepsy (EPM1) patients and cystatin B (CSTB)‐deficient mice, a model system for EPM1. Methods: Tryptophan and its metabolites along serotonin (5‐HT) and KYN pathways were determined in serum of EPM1 patients and CSTB‐deficient mice by reverse‐phase high‐pressure liquid chromatography (HPLC) with electrochemical detection. Results: Reduced levels of 5‐HT and KYN intermediate metabolite 3‐hydroxyanthranilic acid were found in serum of CSTB‐deficient mice. A similar trend was found in EPM1 patients. Although tryptophan concentration was reduced in serum of EPM1 patients, no such decrease was observed in CSTB‐deficient mice. Conclusions: The present study demonstrates that tryptophan metabolism along 5‐HT and KYN pathways are disrupted in EPM1. Further studies are needed to elucidate the role of KYN pathway in pathogenesis of EPM1.