The Journal of Neuroscience, September 29, 2004, ():
Activation of EGL-47, a G
o-Coupled Receptor, Inhibits Function of Hermaphrodite-Specific Motor Neurons to Regulate Caenorhabditis elegans Egg-Laying Behavior
J. Neurosci. Moresco and Koelle
24: 8522
Supplemental data
Files in this Data Supplement:
- supplemental material
-
A model for neurotransmitter signaling in the egg-laying system.
Multiple G protein-coupled receptors activate GOA-1 in the HSN neurons to inhibit neurotransmitter release and thus inhibit egg-laying behavior. Serotonin (5-HT) release from the HSN acts on the egg-laying muscles, via an unidentified receptor, to stimulate contraction and initiate egg laying (Trent et al., 1983). Serotonin also feeds back to activate an unknown autoreceptor (5-HTR) that signals through GOA-1 to limit further neurotransmitter release from the HSN (Shyn et al., 2003). Acetylcholine (ACh) from the VC neurons activates GAR-2 and additional unknown receptors (AChR) on the HSN (Bany et al., 2003). EGL-47 is an additional receptor on the HSN that signals through GOA-1 to inhibit HSN function, however neither the identity nor the source of the EGL-47 ligand has been determined. In addition to acting in the HSN, GOA-1 is found in the egg-laying muscles where it may signal to inhibit contraction (Mendel et al., 1995; Ségalat et al., 1995; Shyn et al., 2003). Since activation of GOA-1 in the HSNs occurs via multiple GPCRs, GOA-1 serves as an integrator of multiple inputs to set the level of egg-laying behavior.
