Title
Inhibition of <tex>$Ca^{2+}$</tex>-sensitive <tex>$K^{+}$</tex> currents in NG 108-15 cells by substance P and related tachykinins Inhibition of <tex>$Ca^{2+}$</tex>-sensitive <tex>$K^{+}$</tex> currents in NG 108-15 cells by substance P and related tachykinins
Author
Faculty/Department
Faculty of Pharmaceutical, Biomedical and Veterinary Sciences . Biomedical Sciences
Publication type
article
Publication
London ,
Subject
Pharmacology. Therapy
Source (journal)
British journal of pharmacology. - London
Volume/pages
119(1996) :2 , p. 315-320
ISSN
0007-1188
ISI
A1996VG29800022
Carrier
E
Target language
English (eng)
Full text (Publishers DOI)
Abstract
1 The whole-cell patch-clamp technique was used to investigate the actions of substance P and other agonists at neurokinin (NK) receptors on voltage-gated K+ and Ca+ channel currents in undifferentiated mouse neuroblastoma x rat glioma NG 108-15 cells. 2 Both substance P (0.3-30 mu M) and the NK1 receptor selective agonist GR73632 (10 nM-10 mu M) caused concentration-dependent inhibition of K+ currents. GR64349 and senktide (agonists at NK2 and NK3 receptors respectively) also inhibited K+ currents, but only at concentrations which were several orders of magnitude greater than GR73632, suggesting that current inhibition was mediated via NK1 receptors. 3 Substance P and GR73632 were without effect on residual K+ currents recorded in the presence of extracellular Co2+ (4 mM) to abolish the Ca2+-sensitive component (IKCa) of the K+ current. Ca2+ channel currents, recorded with either Ba2+ or Ca2+ as charge carrier, were unaffected by NK1, NK2 and NK3 receptor ligands. 4 Iontophoretic application of GR73632 produced a current-dependent reduction of K+ currents. In the presence of the non-peptide NK1 antagonists, CP-99,994 and RP67580, and the peptide antagonist, GR82334, the current-response relationship was reversibly shifted to the right. This indicates that the response is mediated by NK1 receptors. 5 Our results indicate that activation of NK1 receptors leads to the selective inhibition of IKCa in undifferentiated NG 108-15 cells.
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