@article{ref1,
title="Minimal traumatic brain injury in mice: protease-activated receptor 1 and thrombin-related changes",
journal="Journal of neurotrauma",
year="2016",
author="Itsekson-Hayosh, Zeev and Shavit-Stein, Efrat and Katzav, Aviva and Rubovitch, Vardit and Maggio, Nicola and Chapman, Joab and Harnof, Sagi and Pick, Chaim G.",
volume="33",
number="20",
pages="1848-1854",
abstract="Minimal traumatic brain injury (mTBI) is partially defined by the existence of retrograde amnesia and is associated with microscopic bleeds containing activated coagulation factors. In a previous study, we have found that mTBI immediately releases thrombin-like activity in the brain, which induces amnesia by activating protease-activated receptor 1 (PAR-1) and blocking long-term potentiation (LTP). In the present study, we assessed the effects of mTBI on thrombin and PAR-1 levels in the brain using the same model. After the immediate elevation, thrombin activity returned to baseline 1 h post-trauma and increased again 72 h later (42% relative to control; p < 0.005). These changes were associated with a significant increase in PAR-1 levels 24 (17%; p < 0.05) and 72 h (20%; p < 0.05) post-trauma. Interestingly, the late elevation in thrombin-like activity was also associated with elevation of the major central nervous system thrombin inhibitor, protease nexin-1, 72 h post-mTBI (10%; p < 0.005). When thrombin was injected into brain ventricles, an increased sensitivity to seizure-like activity was detected at 72 h post-mTBI. The results are compatible with astrocyte activation post-mTBI resulting in increased thrombin secretion, PAR-1 expression, and seizure sensitivity.<p /> <p>Language: en</p>",
language="en",
issn="0897-7151",
doi="10.1089/neu.2015.4146",
url="http://dx.doi.org/10.1089/neu.2015.4146"
}