IRK-1 Potassium Channels Mediate Peptidergic Inhibition of Caenorhabditis elegans Serotonin Neurons via a Gₒ Signaling Pathway

• Main Authors: Emtage, Lesley (Author), Aziz-Zaman, Sonya (Author), Padovan-Merhar, Olivia (Author), Fang-Yen, Chris (Author), Ringstad, Niels (Author), Horvitz, Howard Robert (Author)
• Other Authors: Massachusetts Institute of Technology. Department of Biology (Contributor), Horvitz, H. Robert (Contributor)
• Format: Article
• Language: English
• Published: Society for Neuroscience, 2013-08-12T19:45:09Z.
• Subjects: Article
• Online Access: Get fulltext

 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.