A neuropeptide-mediated stretch response links muscle contraction to changes in neurotransmitter release |
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Authors: | Hu Zhitao Pym Edward C G Babu Kavita Vashlishan Murray Amy B Kaplan Joshua M |
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Affiliation: | 1 Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA 2 Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA 3 Department of Communication Sciences and Disorders, Emerson College, Boston, MA 02116, USA |
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Abstract: | Although 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. |
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