PT  - JOURNAL ARTICLE
AU  - Lesley Emtage
AU  - Sonya Aziz-Zaman
AU  - Olivia Padovan-Merhar
AU  - H. Robert Horvitz
AU  - Christopher Fang-Yen
AU  - Niels Ringstad
TI  - IRK-1 Potassium Channels Mediate Peptidergic Inhibition of <em>Caenorhabditis elegans</em> Serotonin Neurons via a G<sub>o</sub> Signaling Pathway
AID  - 10.1523/JNEUROSCI.2667-12.2012
DP  - 2012 Nov 14
TA  - The Journal of Neuroscience
PG  - 16285--16295
VI  - 32
IP  - 46
4099  - http://www.jneurosci.org/content/32/46/16285.short
4100  - http://www.jneurosci.org/content/32/46/16285.full
SO  - J. Neurosci.2012 Nov 14; 32
AB  - To identify molecular mechanisms that function in G-protein signaling, we have performed molecular genetic studies of a simple behavior of the nematode Caenorhabditis elegans, egg laying, which is driven by a pair of serotonergic neurons, the hermaphrodite-specific neurons (HSNs). The activity of the HSNs is regulated by the Go-coupled receptor EGL-6, which mediates inhibition of the HSNs by neuropeptides. We report here that this inhibition requires one of three inwardly rectifying K+ channels encoded by the C. elegans genome: IRK-1. Using ChannelRhodopsin-2-mediated stimulation of HSNs, we observed roles for egl-6 and irk-1 in regulating the excitability of HSNs. Although irk-1 is required for inhibition of HSNs by EGL-6 signaling, we found that other Go signaling pathways that inhibit HSNs involve irk-1 little or not at all. These findings suggest that the neuropeptide receptor EGL-6 regulates the potassium channel IRK-1 via a dedicated pool of Go not involved in other Go-mediated signaling. We conclude that G-protein-coupled receptors that signal through the same G-protein in the same cell might activate distinct effectors and that specific coupling of a G-protein-coupled receptor to its effectors can be determined by factors other than its associated G-proteins.