PMID: 7524091Oct 25, 1994Paper

Proteolytic action of thrombin is required for electrical activity-dependent synapse reduction

Proceedings of the National Academy of Sciences of the United States of America
Y LiuP G Nelson

Abstract

Molecular mechanisms of activity-dependent synapse reduction were studied in an in vitro mammalian neuromuscular preparation. Synapse reduction in this model is activity-dependent and is substantially reduced by the broad-spectrum protease inhibitor, leupeptin, suggesting the role of activity-dependent proteolytic action in the process. Our present experiments show that a potent and specific thrombin inhibitor, hirudin, at nanomolar concentration completely blocked the activity-dependent synapse reduction. Furthermore, a naturally occurring serine protease inhibitor, protease nexin I (PNI), which closely colocalizes with acetylcholine receptors at the neuromuscular junction, inhibited the synapse reduction at the same low concentration. In contrast, neither cystatin, a cysteine protease inhibitor, nor aprotinin, a serine protease inhibitor that does not inhibit thrombin, blocked the synapse reduction. Similarly, neither of the inhibitors of the calcium-activated proteases calpain I and II prevented the reduction of synapses. These results strongly suggest that serine proteolytic action by thrombin or thrombin-like molecules is required for synapse reduction in our in vitro model of the mammalian neuromuscular junction.

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Citations

Apr 1, 1997·BioEssays : News and Reviews in Molecular, Cellular and Developmental Biology·Q Chang, R J Balice-Gordon
Oct 1, 1996·Journal of Molecular Neuroscience : MN·B A CitronB W Festoff
Aug 29, 2000·Brain Research. Developmental Brain Research·R W DavenportP G Nelson
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Sep 29, 2012·Proceedings of the National Academy of Sciences of the United States of America·H Shawn JeBai Lu
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Aug 3, 2014·Critical Reviews in Food Science and Nutrition·Yasmine BoudidaAhmed Ouali
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