GDNF is trophic for mouse motoneurons that express a mutant superoxide dismutase (SOD-1) gene.

GDNF is trophic for mouse motoneurons that express a mutant superoxide dismutase (SOD-1) gene.
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GDNF 对表达突变型超氧化物歧化酶 (SOD-1) 基因的小鼠运动神经元具有营养作用。

DOI:
10.1080/14660820050515412
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发表时间:
2000
期刊:
Amyotrophic lateral sclerosis and other motor neuron disorders : official publication of the World Federation of Neurology, Research Group on Motor Neuron Diseases
影响因子:
--
通讯作者:
Bohn,MC
Bohn,MC
中科院分区:
--
文献类型:
--
作者:
Derby,ML;Giuliano,R;Figlewicz,DA;Bohn,MC

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BACKGROUND AND METHODSAn in vitro system of motoneurons was established from mice carrying a transgene for a human superoxide dismutase-1 (SOD-1) with a gly 93 ala mutation that has been characterized and used to compare the effects of glial cell line-derived neurotrophic factor (GDNF) on motoneurons expressing the mutant gene with those on normal motoneurons.RESULTSRecombinant (100 ng/ml) significantly promoted the survival of a subpopulation of choline acetyltransferase (ChAT)-immunoreactive motoneurons that were also immunoreac- tive for the homeoprotein islet-1 in cul- tures from both wild type and mutant SOD-1 mice. However, GDNF did not increase the total number of ChAT-immunoreactive neurons in cultures from either wild type or transgenic mice. A distinct subpopulation of islet- 1-immunoreactive motoneurons charac- terized by a soma 3 1/2 times larger and a ten-fold increase in neurite length was observed exclusively in GDNF-treated cultures. In cultures from mutant SOD-1 mice, there were 3 1/2 times as many motoneurons of this subpopulation as in sclerosis (FALS). These cultures were wild type cultures at 6 days in vitro. In addition, this subpopulation of neurons survived for 10 days in vitro, the longest time point studied, in culture from mutant SOD-1 mice, but not in cultures from wild type mice. This subpopulation was also present at 6 days in vitro in cultures from mutant SOD-1 mice that received GDNF at 3 days in vitro instead of at the time of plating, suggesting that GDNF promotes the differentiation of these neurons.CONCLUSIONOur observations suggest that the expression of a mutant SOD-1 gene, as occurs in familial ALS, does not compromise the trophic effects of GDNF on motoneuron survival, but may affect the development of motoneurons. (ALS 2000: 1:113–122)
DOI: 10.1126/science.8493557
发表时间: 1993-05-21
期刊: SCIENCE
影响因子: 56.9
作者:
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发表时间: 1994
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DOI: --
发表时间: 1994-12
期刊: The American journal of pathology
影响因子: --
作者:
M. C. Canto;M. Gurney
通讯作者: M. C. Canto;M. Gurney