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    Please use this identifier to cite or link to this item: http://nccur.lib.nccu.edu.tw/handle/140.119/99015


    Title: Enhanced GDNF mRNA expression upon (-)-deprenyl and melatonin treatment.
    Authors: 趙知章
    YP, Tang;YL, Ma;CC, Chao;EHY, Lee
    Contributors: 神科所
    Keywords: glial cell line-derived neurotrophic factor;1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine;(−)-deprenyl;GM1 ganglioside;melatonin;gene expression;striatum
    Date: 1998
    Issue Date: 2016-07-13 14:30:49 (UTC+8)
    Abstract: Glial cell line-derived neurotrophic factor (GDNF) has been shown to be a preferentially selective neurotrophic factor for dopamine (DA) neurons. In the present study, we have examined the distribution of GDNF mRNA expression in several major DA-containing cell body and terminal areas and the regulation of GDNF mRNA expression upon various pharmacological treatments. Results indicated that there is a relatively higher GDNF mRNA level in neurons of the nigrostriatal and mesolimbic dopaminergic pathways. Upon chronic 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment (30 mg/kg, i.p., for 7 days), DA level was decreased, whereas GDNF mRNA expression was increased in the striatum, suggesting that more GDNF is synthesized and expressed to cope with the neurotoxin insult. Furthermore, among several DA neuron protective and/or therapeutic agents examined, both intrastriatal injections of (−)-deprenyl (1.25 μg and 2.5 μg) and melatonin (30 μg, 60 μg, and 120 μg) significantly enhanced GDNF mRNA expression in the striatum, whereas the same concentrations of (−)-deprenyl did not affect monoamine oxidase B (MAOB) activity, although it increased glutathione peroxidase (GPx) and/or superoxide dismutase (SOD) activities. Similarly, the same concentrations of melatonin did not alter SOD or GPx activities, except that the highest dose of melatonin (120 μg) increased lipid peroxidation in the striatum. Conversely, GM1 ganglioside injection (45 μg) lacked of an effect on GDNF mRNA expression. Together, these results suggest that both (−)-deprenyl and melatonin up-regulate GDNF gene expression at threshold doses lower than that needed for altering MAOB activity and/or the antioxidant enzyme systems, respectively. These results provide new information on the neuroprotective and therapeutic mechanisms of (−)-deprenyl and melatonin on DA neurons. J. Neurosci. Res. 53:593–604, 1998. © 1998 Wiley-Liss, Inc.
    Relation: J. Neurosci. Res., 53(5), 593-604
    Data Type: article
    DOI link: http://dx.doi.org/10.1002/(SICI)1097-4547(19980901)53:5<593::AID-JNR9>3.0.CO;2-4
    DOI: 10.1002/(SICI)1097-4547(19980901)53:5<593::AID-JNR9>3.0.CO;2-4
    Appears in Collections:[Graduate Institute of Neuroscience] Periodical Articles

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