کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6017998 | 1580183 | 2013 | 5 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The absence of indoleamine 2,3-dioxygenase expression protects against NMDA receptor-mediated excitotoxicity in mouse brain
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کلمات کلیدی
TrpIDO2TDO2IDO1MSNN-methyl-d-aspartateNMDA3-hydroxykynurenine - 3-هیدروکسی ...LC-MS/MS - LC-MS / MSStriatum - استریاتومkynurenic acid - اسید کینورنیکQuinolinic acid - اسید کینولینیکindoleamine 2,3-dioxygenase - ایندولامین 2،3-دیوکسژیگنازHuntington's disease - بیماری هانتینگتونHuntington disease - بیماری هانتینگتونTryptophan - تریپتوفانKYN - جنسیتblood brain barrier - سد خونی مغزیBBB - سد خونی مغزیkynurenine pathway - مسیر kynureninemedium spiny neurons - نورونهای کروی متوسطHuntingtin - هانتینگتنliquid chromatography tandem mass spectrometry - کروماتوگرافی مایع اسپکترومتری دو طرفهkynurenine - کینورینین
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
عصب شناسی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
We previously showed that the expression and activity of indoleamine 2,3-dioxygenase (Ido1) are chronically elevated in the striatum of YAC128 mouse model of HD. This was followed by increased production of neurotoxic metabolite hydroxykynurenine (3-HK) in the striatum of symptomatic mice. We therefore hypothesized that the chronic Ido1 induction in the striatum of YAC128 mice leads to increased neurotoxicity in this mouse model; based on this hypothesis, we predicted that the absence of Ido1 expression would result in decreased sensitivity to neurotoxicity in mice. The work described in this brief communication will include the characterization of Idoâ/â striatum in terms of enzymatic expression and activity in the first step of the pathway. Additionally, we assessed the sensitivity of the striatum to excitotoxic insult in the absence of Ido1 expression in the striatum of constitutive Ido1 null mice (Idoâ/â) and demonstrated that Idoâ/â mice are less sensitive to QA-induced striatal neurotoxicity. Finally, through measurement of kynurenine pathway (KP) metabolites in Idoâ/â mice, we showed decreased levels of 3-HK in the striatum of these mice. This study suggests that the inhibition of the first step in the KP may be neuroprotective and should be considered as a potential therapeutic target in HD and other neurodegenerative diseases.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Neurology - Volume 249, November 2013, Pages 144-148
Journal: Experimental Neurology - Volume 249, November 2013, Pages 144-148
نویسندگان
G. Mazarei, D.P. Budac, G. Lu, H. Lee, T. Möller, B.R. Leavitt,