The messenger RNAs for both glial cell line-derived neurotrophic factor receptors, c- ret and GDNFRα, are induced in the rat brain in response to kainate-induced excitation

The messenger RNAs for both glial cell line-derived neurotrophic factor receptors, c- ret and GDNFRα, are induced in the rat brain in response to kainate-induced excitation
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神经胶质细胞系衍生的神经营养因子受体 c-ret 和 GDNFRα 的信使 RNA 在大鼠大脑中响应红藻氨酸诱导的兴奋而被诱导

DOI:
10.1016/s0306-4522(97)00361-8
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发表时间:
1998
期刊:
影响因子:
3.3
通讯作者:
Mart Saarma
Mart Saarma
中科院分区:
医学3区
文献类型:
--
作者:
Mati Reeben;A. Laurikainen;J. Hiltunen;E. Castrén;Mart Saarma

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胶质细胞源性神经营养因子(GDNF)有两种受体,受体酪氨酸激酶c-ret和糖基磷脂酰肌醇连接的细胞表面受体GDNFRα。红藻氨酸诱导的癫痫发作是一种广泛研究的神经元可塑性和人类癫痫模型,已被证明可以增加大鼠海马中多种营养因子(包括 GDNF)的基因表达。在这里,我们发现全身红藻氨酸诱导的兴奋会导致大鼠大脑中 c-ret 和 GDNFRα 信使 RNA 的短暂增加。 Northern 分析表明,在海马体中,注射红藻氨酸 12 小时后,观察到 c-ret 最大增加 2.5 倍,GDNFRα 信使 RNA 增加 4 倍,而 GDNF 信使 RNA 在 4-6 小时内达到最大值。用放线菌酮阻断蛋白质从头合成可抑制红藻氨酸对 GDNF 受体的诱导,而用拮抗剂马来酸地佐西平阻断 N-甲基-d-天冬氨酸型谷氨酸受体则不会显着改变反应。因此,红藻氨酸对 GDNF 受体信使 RNA 的增加取决于蛋白质合成,但不受 N-甲基-d-天冬氨酸受体介导。红藻氨酸处理后,GDNFRα 和 c-ret 在大脑中显示出不同但部分重叠的表达模式。原位杂交显示,GDNFRα(信使 RNA)在大鼠海马齿状回中显着诱导,在缰核和网状丘脑核以及大脑皮层中诱导较少。 C-ret 转录物在海马门、几个丘脑和杏仁核以及梨状皮层的浅层中被诱导。这些数据表明,GDNF 及其受体可能在神经元可塑性和癫痫损伤后的神经元保护中发挥局部作用。
Glial cell line-derived neurotrophic factor (GDNF) has two receptors, receptor-tyrosine kinase c- ret and glycosylphosphatidylinositol-linked cell surface receptor GDNFRα. Kainate-induced seizures, a widely studied model of neuronal plasticity and human epilepsy, have been shown to increase gene expression of several trophic factors, including GDNF, in the rat hippocampus. Here we show that systemic kainate-induced excitation leads to a transient increase of both c- ret and GDNFRα messenger RNAs in the rat brain. Northern analysis demonstrated that, in the hippocampus, the maximal 2.5-fold increase of c- ret and four-fold increase of GDNFRα messenger RNAs was observed after 12 h of kainate injection, in contrast to GDNF messenger RNA, which reaches its maximum in 4–6 h. The blocking of de novo protein synthesis by cycloheximide inhibited the induction of GDNF receptors by kainate, whereas blocking of the N-methyl- d-aspartate-type glutamate receptors by the antagonist dizocilpine maleate did not significantly alter the response. Thus, GDNF receptor messenger RNA increase by kainate depends on protein synthesis, but is not mediated by the N-methyl- d-aspartate receptor. GDNFRα and c- ret show distinct, but partially overlapping, patterns of expression in the brain after kainate treatment. GDNFRα, messenger RNA was prominently induced in the dentate gyrus of the rat hippocampus, less in the habenular and reticular thalamic nuclei and cerebral cortex as revealed by in situ hybridization. C- ret transcripts were induced in the hilus of the hippocampus, several thalamic and amygdala nuclei and in superficial layers of the piriform cortex. These data suggest that GDNF and its receptors may play a local role in neuronal plasticity and in neuronal protection following epileptic insults.
DOI: 10.1073/pnas.92.18.8274
发表时间: 1995-08
影响因子: 11.1
作者:
A. Tomac;J. Widenfalk;Leu‐Fen H. Lin;Tadahiko Kohno;Ted Ebendal;Barry J. Hoffer;Lars Olson
通讯作者: A. Tomac;J. Widenfalk;Leu‐Fen H. Lin;Tadahiko Kohno;Ted Ebendal;Barry J. Hoffer;Lars Olson
DOI: --
发表时间: 1993-12
期刊: Development
影响因子: 4.6
作者:
V. Pachnis;B. Mankoo;F. Costantini
通讯作者: V. Pachnis;B. Mankoo;F. Costantini
DOI: 10.1016/0165-3806(94)00197-8
发表时间: 1995-03-16
期刊: DEVELOPMENTAL BRAIN RESEARCH
影响因子: --
作者:
CHOILUNDBERG, DL;BOHN, MC
通讯作者: BOHN, MC