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. 2020 Jan 14;10:1532. doi: 10.3389/fphar.2019.01532

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Copyright © 2020 Ben Shimon, Shavit-Stein, Altman, Pick and Maggio

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) 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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Minimal traumatic brain injury (mTBI) lowers the threshold of seizures in the pilocarpine mouse model of status epilepticus through Thrombin-PAR1 mediated excitatory pathway. Thrombin is known to rise in the brain both in hyperexcitable state as well as upon BBB breakdown following mTBI. Thrombin at high concentrations leads to the activation of NMDA receptor through a pathway mediated by PAR1. NMDA receptor activation and the subsequent massive influx of calcium lead to hyperexcitability and lower threshold for seizures to occur.