| Description |
Cell surface Ig superfamily proteins (IgSF) have been implicated in several aspects of neuronal development and function. During the course of my talk I will describe a novel function for a C. elegans IgSF (RIG-3). Mutants lacking rig-3 have an increased paralytic response to aldicarb, a cholinesterase inhibitor. This heightened drug responsiveness in rig-3 mutants was caused by an aldicarb-induced increase in ACR-16 acetylcholine receptor (AChR) abundance at synapses, and a corresponding potentiation of post-synaptic responses. By contrast, aldicarb treatment did not potentiate post-synaptic responses, and had no effect on synaptic ACR-16 abundance in wild type animals. The synaptic potentiation observed in rig-3 mutants was eliminated by mutations that prevent neuropeptide production or secretion, implicating neuropeptides in this form of plasticity. Collectively, our results suggest that the RIG-3 IgSF has an anti-plasticity function, which prevents a form of synaptic potentiation
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