An endogenous RNA transcript antisense to CNGα1 cation channel mRNA

被引:7
作者
Cheng, CH
Yew, DTW
Kwan, HY
Zhou, Q
Huang, Y
Liu, Y
Chan, WY
Yao, XQ [1 ]
机构
[1] Chinese Univ Hong Kong, Fac Med, Dept Physiol, Hong Kong, Hong Kong, Peoples R China
[2] Chinese Univ Hong Kong, Fac Med, Dept Anat, Hong Kong, Hong Kong, Peoples R China
[3] Chinese Univ Hong Kong, Fac Med, Dept Anat & Cellular Pathol, Hong Kong, Hong Kong, Peoples R China
关键词
D O I
10.1091/mbc.E02-03-0127
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
CNG channels are cyclic nucleotide-gated Ca2+-permeable channels that are suggested to be involved in the activity-dependent alterations of synaptic strength that are thought to underlie information storage in the CNS. In this study, we isolated an endogenous RNA transcript antisense to CNGalpha1 mRNA. This transcript was capable of down-regulating the expression of sense CNGalpha1 in the Xenopus oocyte expression system. RT-PCR, Northern blot, and in situ hybridization analyses showed that the transcript was coexpressed with CNGalpha1 mRNA in many regions of human brain, notably in those regions that were involved in long-term potentiation and long-term depression, such as hippocampal CA1 and CA3, dentate gyrus, and cerebellar Purkinje layer. Comparison of expression patterns between adult and fetal cerebral cortex revealed that there were concurrent developmental changes in the expression levels of anti-CNG1 and CNGalpha1. Treatment of human glioma cell T98 with thyroid hormone T-3 caused a significant increase in anti-CNG1 expression and a parallel decrease in sense CNGalpha1 expression. These data suggest that the suppression of CNGalpha1 expression by anti-CNG1 may play an important role in neuronal functions, especially in synaptic plasticity and cortical development. Endogenous antisense RNA-mediated regulation may represent a new mechanism through which the activity of ion channels can be regulated in the human CNS.
引用
收藏
页码:3696 / 3705
页数:10
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