日志
翻译下我发表在《神经科学杂志》上的文章
热度 1 ||
这是应论坛网友要求做的，感觉把一些英文的术语翻译成中文还真是不容易，希望大家能及时指出错误。
中文摘要如下：
题目：在体研究GABAA受体依赖的突触传递对树突形态结构的影响
作者：沈万华，DA SILVA JS, HE HAIYAN, CLINE HT.
树突结构的产生依赖于其它突触的输入。我们想证明如下设想：抑制性GABA能突触传递是否能调节早蟾视顶盖细胞的树突发育。因为GABA受体的gamma2亚基有一段细胞内的跨膜端序列，这段序列对锚定GABAA受体到突触后膜是必须的，所以我们的主要方法是设计了一段特异性的争对细胞内段的序列（ICL），这样就特异性的阻断了单个细胞GABA能的突触传递。免疫组化实验证明了EGFP-ICL是以PUNCTA的形式分布于抑制性神经元的树突上。电生理结果发现，有大约36%的EGFP-ICL转染的神经元没有GABA能介导的突触传递，而且余下的约64%的EGFP-ICL转染的神经元的mIPSCs的频率也比对照组低。但ICL转染的神经元不影响谷氨酸能突触传递，也不影响突触前神经元的递质释放概率或神经元的兴奋性。苯二氮卓受体阻断药对EGFP-ICL转染神经元的GABA能诱发电流的增强作用也受到抑制，说明EGFP-ICL的转染是特异性的阻断gamma2亚基的转运上膜。ICL的磷酸化位点突变体和对照组一样证明了EGFP-ICL的特异性。活细胞长期观察实验证明，EGFP-ICL细胞的树突总面积比对照组增大，而树突的分枝减少。活细胞动态实验证明，ICL转染会降低树突分枝的分叉速度。而且我们还发现，GABA能突触传递的抑制会降低细胞视觉经验依赖的树突结构可塑性。综上所述，我们的早蟾在体研究证实了这样的一个必须机制，抑制性的突触传递在调节树突结构可塑性的过程中起着非常重要的角色。
英文摘要如下：
1: J Neurosci. 2009 Apr 15;29(15):5032-43.
Links
Type A GABA-receptor-dependent synaptic transmission sculpts dendritic arbor structure in Xenopus tadpoles in vivo. Shen W, Da Silva JS, He H, Cline HT.
Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA.
The emergence of dendritic arbor structure in vivo depends on synaptic inputs. We tested whether inhibitory GABAergic synaptic transmission regulates Xenopus optic tectal cell dendritic arbor development in vivo by expressing a peptide corresponding to an intracellular loop (ICL) ofthe gamma2 subunit of type A GABA receptors (GABA(A)R), which is required to anchor GABA(A) receptors to the postsynaptic scaffold.Enhanced green fluorescent protein (EGFP)-tagged ICL (EGFP-ICL) was distributed in a punctate pattern at putative inhibitory synapses,identified by vesicular GABA transporter immunoreactive puncta. ICL expression completely blocked GABA(A)R-mediated transmission in 36% of transfected neurons and significantly reduced GABA(A)R-mediated synaptic currents relative to AMPA receptor-mediated synaptic currentsin the remaining transfected neurons without altering release probability or neuronal excitability. Further analysis of ICL-expressing neurons with residual GABA(A)R-mediated inputs showed that the capacity of benzodiazepine to enhance GABAergic synaptic responses was reduced in ICL-expressing neurons, indicating that they were likely depleted of gamma2 subunit-containing GABA(A)R. Neurons expressing a mutant form of ICL were comparable to controls. In vivo time-lapse images showed that ICL-expressing neurons have more sparsely branched dendritic arbors, which expand over larger neuropil areas than EGFP-expressing control neurons. Analysis of branch dynamics indicated that ICL expression affected arbor growth by reducing rates of branch addition. Furthermore, we found that decreasing GABAergic synaptic transmission with ICL expression blocked visual experience dependent dendritic arbor structural plasticity. Our findings establish an essential role for inhibitory GABAergic synaptic transmission in the regulation of dendritic structural plasticity in Xenopus in vivo.
PMID: 19369572 [PubMed - in process]
中文摘要如下：
题目：在体研究GABAA受体依赖的突触传递对树突形态结构的影响
作者：沈万华，DA SILVA JS, HE HAIYAN, CLINE HT.
树突结构的产生依赖于其它突触的输入。我们想证明如下设想：抑制性GABA能突触传递是否能调节早蟾视顶盖细胞的树突发育。因为GABA受体的gamma2亚基有一段细胞内的跨膜端序列，这段序列对锚定GABAA受体到突触后膜是必须的，所以我们的主要方法是设计了一段特异性的争对细胞内段的序列（ICL），这样就特异性的阻断了单个细胞GABA能的突触传递。免疫组化实验证明了EGFP-ICL是以PUNCTA的形式分布于抑制性神经元的树突上。电生理结果发现，有大约36%的EGFP-ICL转染的神经元没有GABA能介导的突触传递，而且余下的约64%的EGFP-ICL转染的神经元的mIPSCs的频率也比对照组低。但ICL转染的神经元不影响谷氨酸能突触传递，也不影响突触前神经元的递质释放概率或神经元的兴奋性。苯二氮卓受体阻断药对EGFP-ICL转染神经元的GABA能诱发电流的增强作用也受到抑制，说明EGFP-ICL的转染是特异性的阻断gamma2亚基的转运上膜。ICL的磷酸化位点突变体和对照组一样证明了EGFP-ICL的特异性。活细胞长期观察实验证明，EGFP-ICL细胞的树突总面积比对照组增大，而树突的分枝减少。活细胞动态实验证明，ICL转染会降低树突分枝的分叉速度。而且我们还发现，GABA能突触传递的抑制会降低细胞视觉经验依赖的树突结构可塑性。综上所述，我们的早蟾在体研究证实了这样的一个必须机制，抑制性的突触传递在调节树突结构可塑性的过程中起着非常重要的角色。
英文摘要如下：
1: J Neurosci. 2009 Apr 15;29(15):5032-43.
LinksType A GABA-receptor-dependent synaptic transmission sculpts dendritic arbor structure in Xenopus tadpoles in vivo. Shen W, Da Silva JS, He H, Cline HT.
Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA.
The emergence of dendritic arbor structure in vivo depends on synaptic inputs. We tested whether inhibitory GABAergic synaptic transmission regulates Xenopus optic tectal cell dendritic arbor development in vivo by expressing a peptide corresponding to an intracellular loop (ICL) ofthe gamma2 subunit of type A GABA receptors (GABA(A)R), which is required to anchor GABA(A) receptors to the postsynaptic scaffold.Enhanced green fluorescent protein (EGFP)-tagged ICL (EGFP-ICL) was distributed in a punctate pattern at putative inhibitory synapses,identified by vesicular GABA transporter immunoreactive puncta. ICL expression completely blocked GABA(A)R-mediated transmission in 36% of transfected neurons and significantly reduced GABA(A)R-mediated synaptic currents relative to AMPA receptor-mediated synaptic currentsin the remaining transfected neurons without altering release probability or neuronal excitability. Further analysis of ICL-expressing neurons with residual GABA(A)R-mediated inputs showed that the capacity of benzodiazepine to enhance GABAergic synaptic responses was reduced in ICL-expressing neurons, indicating that they were likely depleted of gamma2 subunit-containing GABA(A)R. Neurons expressing a mutant form of ICL were comparable to controls. In vivo time-lapse images showed that ICL-expressing neurons have more sparsely branched dendritic arbors, which expand over larger neuropil areas than EGFP-expressing control neurons. Analysis of branch dynamics indicated that ICL expression affected arbor growth by reducing rates of branch addition. Furthermore, we found that decreasing GABAergic synaptic transmission with ICL expression blocked visual experience dependent dendritic arbor structural plasticity. Our findings establish an essential role for inhibitory GABAergic synaptic transmission in the regulation of dendritic structural plasticity in Xenopus in vivo.
PMID: 19369572 [PubMed - in process]
