PT  - JOURNAL ARTICLE
AU  - Hideyuki Murakoshi
AU  - James S. Trimmer
TI  - Identification of the Kv2.1 K&lt;sup&gt;+&lt;/sup&gt; Channel as a Major Component of the Delayed Rectifier K&lt;sup&gt;+&lt;/sup&gt; Current in Rat Hippocampal Neurons
AID  - 10.1523/JNEUROSCI.19-05-01728.1999
DP  - 1999 Mar 01
TA  - The Journal of Neuroscience
PG  - 1728--1735
VI  - 19
IP  - 5
4099  - http://www.jneurosci.org/content/19/5/1728.short
4100  - http://www.jneurosci.org/content/19/5/1728.full
SO  - J. Neurosci.1999 Mar 01; 19
AB  - Molecular cloning studies have revealed the existence of a large family of voltage-gated K+ channel genes expressed in mammalian brain. This molecular diversity underlies the vast repertoire of neuronal K+ channels that regulate action potential conduction and neurotransmitter release and that are essential to the control of neuronal excitability. However, the specific contribution of individual K+ channel gene products to these neuronal K+ currents is poorly understood. We have shown previously, using an antibody, “KC,” specific for the Kv2.1 K+ channel α-subunit, the high-level expression of Kv2.1 protein in hippocampal neurons in situ and in culture. Here we show that KC is a potent blocker of K+ currents expressed in cells transfected with the Kv2.1 cDNA, but not of currents expressed in cells transfected with other highly related K+ channel α-subunit cDNAs. KC also blocks the majority of the slowly inactivating outward current in cultured hippocampal neurons, although antibodies to two other K+ channel α-subunits known to be expressed in these cells did not exhibit blocking effects. In all cases the blocking effects of KC were eliminated by previous incubation with a recombinant fusion protein containing the KC antigenic sequence. Together these studies show that Kv2.1, which is expressed at high levels in most mammalian central neurons, is a major contributor to the delayed rectifier K+ current in hippocampal neurons and that the KC antibody is a powerful tool for the elucidation of the role of the Kv2.1 K+ channel in regulating neuronal excitability.