Expression of a non-inactivating K+ channel driven by a rat heat shock promoter increased the resting potential in Aplysia silent neurons.
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.
Institute of Molecular Biology and Genetics, Department of Biology, College of Natural Sciences, Seoul National University, South Korea.
J H
JH
Han
S W
SW
Yim
C S
CS
Lim
C W
CW
Park
B K
BK
Kaang
D000818:Animals; D001048:Aplysia; D002478:Cells, Cultured; D004790:Enzyme Induction; D018840:HSP70 Heat-Shock Proteins / Q000235:genetics* / Q000378:metabolism; D006358:Hot Temperature; D007763:Lac Operon; D008564:Membrane Potentials / Q000235:genetics* / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D010957:Plasmids / Q000235:genetics; D015221:Potassium Channels / Q000235:genetics* / Q000378:metabolism; D051381:Rats; D001616:beta-Galactosidase / Q000235:genetics / Q000378:metabolism
D018840:HSP70 Heat-Shock Proteins; D015221:Potassium Channels; D001616:beta-Galactosidase