Minimal Traumatic Brain Injury in Mice: Protease-Activated Receptor 1 and Thrombin-Related Changes
Minimal Traumatic Brain Injury in Mice: Protease-Activated Receptor 1 and Thrombin-Related Changes
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DOI：
10.1089/neu.2015.4146
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发表时间：
2016-10-15
影响因子：
4.2
通讯作者：
Pick, Chaim G.
中科院分区：
文献类型：
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作者：
Itsekson-Hayosh, Zeev;Shavit-Stein, Efrat;Pick, Chaim G.
轻微创伤性脑损伤（mTBI）部分定义为逆行性遗忘症的存在，并与含有活化凝血因子的显微镜下出血相关。在先前的研究中，我们发现mTBI立即在大脑中释放凝血酶样活性，其通过激活蛋白酶激活受体1（PAR-1）和阻断长时程增强（LTP）诱导健忘症。在本研究中，我们使用相同的模型评估了mTBI对脑中凝血酶和PAR-1水平的影响。在创伤后即刻升高后，凝血酶活性在创伤后1小时恢复到基线水平，并在72小时后再次升高（相对于对照组为42%; p
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 1h post-trauma and increased again 72h later (42% relative to control; p