کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10299262 | 539700 | 2014 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
d-cycloserine lowers kynurenic acid formation-New mechanism of action
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کلمات کلیدی
d-cycloserineEAAN-methyl-d-aspartateNMDA2-amino-2-methyl-1-propanol - 2-آمینو-2-متیل-1-پروپانولNMDA receptor - NMDA گیرندهexcitatory amino acid - آمینو اسید هیجان انگیزkynurenic acid - اسید کینورنیکDementia - جنون یا زوال عقلNumber - عددHIV-1 - ویروس اچ آی وی نوع یکHuman Immunodeficiency Virus type-1 - ویروس ایمنی بدن نوع 1HIV - ویروس نقص ایمنی انسانی KAT - کتKYNA - کیاناkynurenine aminotransferases - کینورینین آمینوترانسفرازKynurenine aminotransferase - کینورینین آمینوترانسفرازGlycine - گلیسین
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
روانپزشکی بیولوژیکی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
d-Cycloserine, known as a partial agonist at the glycine modulatory site of the glutamatergic N-methyl-d-aspartate (NMDA) receptor, exerts anticonvulsive activities and improves cognitive function. The present study evaluates the action of d-cycloserine with respect to the biosynthetic machinery of kynurenic acid (KYNA) synthesis e.g. the activity of enzymes synthesizing KYNA, kynurenine aminotransferases I, kynurenine aminotransferase II and kynurenine aminotransferase III (KAT I, KAT II and KAT III) in the rat liver and brain, and human frontal cortex in the presence of the anti-mycobacterial drug d-cycloserine, in an in vitro study. We found that d-cycloserine blocked dose-dependent and significantly KAT I, II and III activities in rat liver and brain homogenates. Furthermore, the inhibitory effect of KYNA formation was observed in the frontal cortex homogenate of human post mortem tissue, as well. d-Cycloserine, at 63.7 µM concentration blocked significantly KAT II, I and III (53.2, 66.1 and 71.3% of control, P<0.001) activities in the human frontal cortex homogenate. Obtained data indicate that d-cycloserine exerts notable biochemical properties to block KYNA synthesis. Lowering of KYNA content due to d-cycloserine inhibition of KATs activities can free up more glycine sites for the actions of d-cycloserine. On the other site, it needs to be clarified, if the postulated mechanism for d-cycloserine to act as a partial agonist at the glycine site of the NMDA receptor could be mainly due to KAT's inhibition. We propose that this mechanism(s) might play a role in the improvement of memory, cognition and/or delusion in Alzheimer's, HIV-1 infected patients and schizophrenia patients.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: European Neuropsychopharmacology - Volume 24, Issue 4, April 2014, Pages 639-644
Journal: European Neuropsychopharmacology - Volume 24, Issue 4, April 2014, Pages 639-644
نویسندگان
Halina Baran, Berthold Kepplinger,