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. 2015 Apr 21;9:151. doi: 10.3389/fncel.2015.00151

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Copyright © 2015 Ben Shimon, Lenz, Ikenberg, Becker, Shavit Stein, Chapman, Tanne, Pick, Blatt, Neufeld, Vlachos and Maggio.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution and reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Concentration-dependent effects of thrombin on synaptic plasticity. High levels of thrombin cause a slow onset NMDAR-dependent LTP by direct activation of PAR1. Low concentrations of thrombin activate Protein C which binds to EPCR and activates PAR1 to induce metaplasticity, i.e., a reduction in the LTP threshold [by recruitment of L-type voltage gated calcium channels (L-VGCC), metabotropic glutamate receptors 5 (mGluR5), sphingosine-1-phosphate (S1P), and internal calcium stores]. For further details refer to the main text and Maggio et al. (2013c).