Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
4321470 | Neuron | 2011 | 11 Pages |
SummaryAlthough Caenorhabditis elegans has been utilized extensively to study synapse formation and function, relatively little is known about synaptic plasticity in C. elegans. We show that a brief treatment with the cholinesterase inhibitor aldicarb induces a form of presynaptic potentiation whereby ACh release at neuromuscular junctions (NMJs) is doubled. Aldicarb-induced potentiation was eliminated by mutations that block processing of proneuropeptides, by mutations inactivating a single proneuropeptide (NLP-12), and by those inactivating an NLP-12 receptor (CKR-2). NLP-12 expression is limited to a single stretch-activated neuron, DVA. Analysis of a YFP-tagged NLP-12 suggests that aldicarb stimulates DVA secretion of NLP-12. Mutations disrupting the DVA mechanoreceptor (TRP-4) decreased aldicarb-induced NLP-12 secretion and blocked aldicarb-induced synaptic potentiation. Mutants lacking NLP-12 or CKR-2 have decreased locomotion rates. Collectively, these results suggest that NLP-12 mediates a mechanosensory feedback loop that couples muscle contraction to changes in presynaptic release, thereby providing a mechanism for proprioceptive control of locomotion.
► A cholinesterase inhibitor (aldicarb) induces presynaptic potentiation ► Synaptic potentiation is mediated by a neuropeptide (NLP-12) and its receptor (CKR-2) ► Aldicarb stimulates NLP-12 release from a stretch-sensing neuron (DVA) ► The NLP-12 proprioceptive feedback loop is required to sustain high locomotion rates