ArticleThe Journal of physiology2002
Activation of a PTX-insensitive G protein is involved in histamine-induced recombinant M-channel modulation.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Serotonin 5-HT2C receptor-mediated inhibition of the M-current in hypothalamic POMC neurons.American journal of physiology. Endocrinology and metabolism · 2012Article
- The cannabinoid WIN 55,212-2 inhibits transient receptor potential vanilloid 1 (TRPV1) and evokes peripheral antihyperalgesia via calcineurin.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
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2 authors.
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Abstract
The M-type potassium current (I(M)) plays a dominant role in regulating membrane excitability and is modulated by many neurotransmitters. However, except in the case of bradykinin, the signal transduction pathways involved in M-channel modulation have not been fully elucidated. The channels underlying I(M) are produced by the coassembly of KCNQ2 and KCNQ3 channel subunits and can be expressed in heterologous systems where they can be modulated by several neurotransmitter receptors including histamine H(1) receptors. In HEK293T cells, histamine acting via transiently expressed H(1)R produced a strong inhibition of recombinant M-channels but had no overt effects on the voltage dependence or voltage range of I(M) activation. In addition, the modulation of I(M) by histamine was not voltage sensitive, whereas channel gating, particularly deactivation, was accelerated by histamine. Non-hydrolysable guanine nucleotide analogues (GDP-beta-S and GTP-gamma-S) and pertussis toxin (PTX) treatment demonstrated the involvement of a PTX-insensitive G protein in the signal transduction pathway mediating histamine-induced I(M) modulation. Abrogation of the histamine-induced modulation of I(M) by expression of a C-terminal construct of phospholipase C (PLC-beta1-ct), which buffers activated Galpha(q/11) subunits, implicates this G protein alpha subunit in the modulatory pathway. On the other hand, abrogation of the histamine-induced modulation of I(M) by expression of two constructs which buffer free betagamma subunits, transducin (Galphat) and a C-terminal construct of a G protein receptor kinase (MAS-GRK2-ct), implicates betagamma dimers in the modulatory pathway. These findings demonstrate that histamine modulates recombinant M-channels in HEK293T cells via a PTX-insensitive G protein, probably Galpha(q/11), in a similar manner to a number of other G protein-coupled receptors. However, histamine-induced I(M) modulation in HEK293T cells is novel in that betagamma subunits in addition to Galpha(q/11) subunits appear to be involved in the modulation of KCNQ2/3 channel currents.
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