Two types of K(+) channel subunit, Erg1 and KCNQ2/3, contribute to the M-like current in a mammalian neuronal cell

被引:0
作者
Selyanko, AA
Hadley, JK
Wood, IC
Abogadie, FC
Delmas, P
Buckley, NJ
London, B
Brown, DA
机构
[1] UCL, Dept Pharmacol, London WC1E 6BT, England
[2] UCL, Wellcome Lab Mol Pharmacol, London WC1E 6BT, England
[3] Univ Pittsburgh, Med Ctr, Cardiovasc Inst, Pittsburgh, PA 15213 USA
基金
英国惠康基金;
关键词
potassium channels; neuroblastoma x glioma hybrid cells; M current; sympathetic neuron; Erg1; KCNQ;
D O I
暂无
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The potassium M current was originally identified in sympathetic ganglion cells, and analogous currents have been reported in some central neurons and also in some neural cell lines. It has recently been suggested that the M channel in sympathetic neurons comprises a heteromultimer of KCNQ2 and KCNQ3 (Wang et al., 1998) but it is unclear whether all other M-like currents are generated by these channels. Here we report that the M-like current previously described in NG108-15 mouse neuroblastoma x rat glioma cells has two components, "fast" and "slow", that may be differentiated kinetically and pharmacologically. We provide evidence from PCR analysis and expression studies to indicate that these two components are mediated by two distinct molecular species of K(+) channel: the fast component resembles that in sympathetic ganglia and is probably carried by KCNQ2/3 channels, whereas the slow component appears to be carried by merg1a channels. Thus, the channels generating M-like currents in different cells may be heterogeneous in molecular composition.
引用
收藏
页码:7742 / 7756
页数:15
相关论文
共 54 条
[1]  
Abogadie F C, 1997, Methods Mol Biol, V83, P217
[2]   REDUCTION OF SPIKE FREQUENCY ADAPTATION AND BLOCKADE OF M-CURRENT IN RAT CA1 PYRAMIDAL NEURONS BY LINOPIRDINE (DUP-996), A NEUROTRANSMITTER RELEASE ENHANCER [J].
AIKEN, SP ;
LAMPE, BJ ;
MURPHY, PA ;
BROWN, BS .
BRITISH JOURNAL OF PHARMACOLOGY, 1995, 115 (07) :1163-1168
[3]   Modulation of human erg K+ channel gating by activation of a G protein-coupled receptor and protein kinase C [J].
Barros, F ;
Gómez-Varela, D ;
Viloria, CG ;
Palomero, T ;
Giráldez, T ;
de la Peña, P .
JOURNAL OF PHYSIOLOGY-LONDON, 1998, 511 (02) :333-346
[4]   CHARACTERIZATION OF MUSCARINIC RECEPTOR SUBTYPES INHIBITING CA2+ CURRENT AND M-CURRENT IN RAT SYMPATHETIC NEURONS [J].
BERNHEIM, L ;
MATHIE, A ;
HILLE, B .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1992, 89 (20) :9544-9548
[5]  
Bianchi L, 1998, CANCER RES, V58, P815
[6]   A potassium channel mutation in neonatal human epilepsy [J].
Biervert, C ;
Schroeder, BC ;
Kubisch, C ;
Berkovic, SF ;
Propping, P ;
Jentsch, TJ ;
Steinlein, OK .
SCIENCE, 1998, 279 (5349) :403-406
[7]  
Brown D A, 1988, Ion Channels, V1, P55
[8]   INOSITOL 1,4,5-TRISPHOSPHATE AND DIACYLGLYCEROL MIMIC BRADYKININ EFFECTS ON MOUSE NEUROBLASTOMAXRAT GLIOMA HYBRID-CELLS [J].
BROWN, DA ;
HIGASHIDA, H .
JOURNAL OF PHYSIOLOGY-LONDON, 1988, 397 :185-207
[9]   MUSCARINIC SUPPRESSION OF A NOVEL VOLTAGE-SENSITIVE K+ CURRENT IN A VERTEBRATE NEURON [J].
BROWN, DA ;
ADAMS, PR .
NATURE, 1980, 283 (5748) :673-676
[10]   VOLTAGE-ACTIVATED AND CALCIUM-ACTIVATED POTASSIUM CURRENTS IN MOUSE NEUROBLASTOMAXRAT GLIOMA HYBRID-CELLS [J].
BROWN, DA ;
HIGASHIDA, H .
JOURNAL OF PHYSIOLOGY-LONDON, 1988, 397 :149-165