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Histamine inhibits KCNQ2/KCNQ3 channel current via recombinant histamine H(1) receptors.

Juan Guo, Geoffery G Schofield

Neurosci. Lett., 2002 Aug 16 , 328, 285-8

A variety of agonists are capable of inhibiting M-type K(+) channels via the activation of G-protein coupled receptors which converge on phospholipase-C (PLC) via the activation of G(q/11). Histamine acting via H(1) receptors also activates PLC but to date has not been shown to produce M-current (I(M)) modulation. We postulated that histamine would modulate recombinant M-channels after expressing histamine H(1) receptors in heterologous systems. Expression of KCNQ2 and KCNQ3 K(+) channel subunits by transient transfection in HEK 293T and HeLa cells caused the induction of a slow time-dependent outward current characteristic of I(M). Application of histamine (10 microM) to cells transfected with KCNQ2 and KCNQ3 K(+) channel subunits and H(1) histamine receptors produced a rapid and reversible inhibition. I(M) modulation by histamine was concentration-dependent, half maximal inhibition occurring at 399 nM with a Hill coefficient of 1.09 and was completely abolished by the H(1) receptor selective antagonist, astemizole. Studies of the modulatory effects of histamine on I(M) may aid in elucidating the signal transduction pathway(s) involved in I(M) modulation.

http://www.ncbi.nlm.nih.gov/pubmed/12147327