Neurexin and Neuroligin Mediate Retrograde Synaptic Inhibition in C. elegans
Author(s) -
Zhitao Hu,
Sabrina L. Hom,
Tambudzai Kudze,
Xia-Jing Tong,
Seungwon Choi,
Gayane Aramuni,
Weiqi Zhang,
Joshua M. Kaplan
Publication year - 2012
Publication title -
science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 12.556
H-Index - 1186
eISSN - 1095-9203
pISSN - 0036-8075
DOI - 10.1126/science.1224896
Subject(s) - neuroligin , neurexin , neuroscience , neurotransmission , synaptic vesicle , microbiology and biotechnology , inhibitory postsynaptic potential , neurotransmitter , caenorhabditis elegans , schizophrenia (object oriented programming) , chemistry , biology , excitatory postsynaptic potential , gene , medicine , biochemistry , postsynaptic potential , central nervous system , psychiatry , vesicle , receptor , membrane
The synaptic adhesion molecules neurexin and neuroligin alter the development and function of synapses and are linked to autism in humans. Here, we found that Caenorhabditis elegans neurexin (NRX-1) and neuroligin (NLG-1) mediated a retrograde synaptic signal that inhibited neurotransmitter release at neuromuscular junctions. Retrograde signaling was induced in mutants lacking a muscle microRNA (miR-1) and was blocked in mutants lacking NLG-1 or NRX-1. Release was rapid and abbreviated when the retrograde signal was on, whereas release was slow and prolonged when retrograde signaling was blocked. The retrograde signal adjusted release kinetics by inhibiting exocytosis of synaptic vesicles (SVs) that are distal to the site of calcium entry. Inhibition of release was mediated by increased presynaptic levels of tomosyn, an inhibitor of SV fusion.
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