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Neurosci Res. 2002 Jan;42(1):7-14.

Genes responsible for native depolarization-activated K+ currents in neurons.

Author information

1
Department of Electronic Engineering, Graduate School of Engineering, Osaka University, 2-1 Yamadaoka, Suita 565-0871, Japan. song@ele.eng.osaka-u.ac.jp

Abstract

Depolarization-activated, Ca2+-independent K+ currents can be largely divided into delayed rectifiers and transient A-type currents. In mammals, each of these subtypes exhibits large variations in voltage dependence and kinetics according to cell types. At the molecular level, the principal subunits of depolarization-activated K+ channels are thought to be coded by genes from nine subfamilies, Kv1 through Kv9, of which members within each of the Kv1-Kv4 subfamilies can form either homomeric or heteromeric, functional tetrameric channels. The variations in current properties and the large number of genes make it difficult to identify genes responsible for native K(+) channels in mammalian neurons. Nevertheless, progress has been made in recent years, in which the single cell/reverse transcription/polymerase chain reaction (scRT-PCR) protocol combined with patch clamp recording played important roles. With this technique, it has been shown in a number of neuronal phenotypes that mammalian neurons create diversity of channel function by coexpression of members of different Kv subfamilies, coexpression of multiple members of a Kv subfamily, and coexpression of multiple principal and auxiliary subunits. Some genes appear to be expressed at higher levels than others. In the somatodendritic domain, evidence is accumulating that Kv4 subfamily is a major contributor for the typical A-type current, while delayed rectifiers are often attributable to Kv2 and Kv3 subfamily genes. It thus appears that mammalian neurons express some particular Kv genes at higher levels while coexpress multiple genes for the composition of depolarization-activated K+ channels. In addition to the evolution of a large number of K+ channel genes, coexpression of multiple members of the genes in a single neuron also appears to be a strategy for mammalian neurons to create channel diversity.

PMID:
11814604
DOI:
10.1016/s0168-0102(01)00305-4
[Indexed for MEDLINE]

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