NLP-1, a buccalin-related peptide, is expressed in a chemosensory neuron and acts upon the NPR-11 receptor
in an interneuron to modulate the dynamics of the odor-evoked response in that same chemosensory neuron, suggesting the existence of a feedback connection between the interneuron and the chemosensory neuron (Chalasani et al., 2010). This feedback connection is mediated by an insulin-related peptide (INS-1) secreted by the interneuron (Chalasani et al., 2010). The NLP-12 peptide is expressed specifically this website in a stretch receptor neuron, and loss-of-function mutants of nlp-12 or its receptor (ckr-2) eliminate pharmacologically induced presynaptic potentiation of ACh release at the neuromuscular junction and result
in decreased locomotion rates ( Hu et al., 2011). In addition, imaging analysis of fluorescently tagged NLP-12 suggests that its secretion is stimulated by the pharmacological agent that induces presynaptic potentiation and that stimulation is prevented by a TRP channel mutation that disrupts mechanosensation in the stretch receptor ( Hu et al., 2011). These results support a model in which NLP-12 mediates a feedback loop that couples motor-induced activation of a stretch receptor to the strength of the neuromuscular junction, although future work is required to identify the cellular locus and molecular mechanisms by which CKR-2 receptor activation closes the loop. Neuropeptides also modulate worm reproductive behaviors, including egg laying and copulation. Neuropeptides encoded by the Screening Library flp-1 gene (the first worm neuropeptide gene whose mutation was shown to induce behavioral defects; Nelson et al., 1998) promote transition from the behavioral state of egg retention to active egg laying, as flp-1 loss-of-function mutant worms spend longer in the egg-retaining state than wild-type
worms ( Waggoner et al., 2000). FLP-1 peptide regulation of egg-laying is bidirectional, as flp-1 mutant worms also fail to suppress egg-laying in food-poor environments ( Waggoner et al., 2000). Egg-laying behavior is also modulated by the EGL-6 neuropeptide receptor whose ligands are related FaRPs encoded by the flp-10 and flp-17 genes ( Ringstad and Horvitz, 2008). Terminal deoxynucleotidyl transferase These peptides are expressed in sensory neurons that inhibit egg-laying, as when they are ablated, egg-laying is increased, whereas egl-6 is expressed in motor neurons that innervate egg-laying muscles ( Ringstad and Horvitz, 2008). This leads to a simple model in which sensory stimuli relevant to the suitability of the environment for egg-laying control FLP-10/FLP-17 secretion, which directly modulates the activity of the egg-laying motor neurons to promote egg-laying in suitable environments and suppress it when unsuitable.