Expression of a non-inactivating K+ channel driven by a rat heat shock promoter increased the resting potential in Aplysia silent neurons

被引:4
作者
Han, JH
Yim, SW
Lim, CS
Park, CW
Kaang, BK [1 ]
机构
[1] Seoul Natl Univ, Mol Neurobiol Lab, Inst Mol Biol & Genet, Dept Biol,Coll Nat Sci, Seoul 151742, South Korea
[2] Korea Inst Sci & Technol, Biomed Res Ctr, Seoul 130650, South Korea
关键词
non-inactivating K+ channel; Aplysia neuron; heat shock promoter; transgenic expression; resting potential; DNA microinjection;
D O I
10.1016/S0168-0102(99)00027-9
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
We assessed the role of a non-inactivating K+ channel (aKv5.1) in the resting potential by overexpressing this channel by heat shock in the neurons. A reporter gene lacZ linked to a promoter region spanning from the - 285 to the + 88 base of the rat HSP70ib gene was induced 62.5-fold when this DNA construct was microinjected into the neurons of the marine mollusk Aplysia and treated with heat shock at 30 degrees C for 3 h. Using this efficient induction system, we induced the expression of aKv5.1 by heat shock in cultured, electrically silent neurons of Aplysia and examined its effect on the resting potential. The channel expression increased the resting potential by approximately 10 mV. This increase was specific to heat shock induction and abolished by treatment with TEA, a specific K+ channel blocker. These results provide the direct evidence that a low voltage-activated, non-inactivating K+ channel can contribute to the resting potential. (C) 1999 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:13 / 19
页数:7
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