OBSERVATION ON BRAIN-DERIVED NEUROTROPHIC FACTOR IN CEREBRAL ISCHEMIA

我们的研究通常集中在防御性的性质， 再生机制，可以激活响应缺血 以及对这种损伤潜在治疗操作 防御性反应。 在这些研究中，我们能够证明 BDNF参与增强的神经元发育 对缺血性损伤的抗性，在诱导后3天可证实， 将抑郁扩散到大脑皮层 在治疗试验中， 通过立体定向插入腹侧的微导管给药 心脏骤停脑缺血大鼠丘脑区 （CACI）。BDNF的递送在CACI前3天开始， 持续至心脏骤停后7天处死动物。 利用GABA的特异性单克隆抗体， 腹侧GABA能终末的增殖和出芽 在BDNF递送位点附近的丘脑核。 还有， 核中GABA能神经元的保护是一个阴谋 应用BDNF一侧的网状丘脑。

Our studies have generally been focused on the nature of defensive and regenerative mechanisms which can be activated in response to ischemic injury, as well as on potential therapeutic manipulation of such defensive responses. In these studies we were able to demonstrate participation of the BDNF in the development of enhanced neuronal resistance to ischemic injury, demonstrable 3 days after induction of the spreading depression to the cortex. In therapeutic trials, BDNF was administered via the microcanule inserted sterotaxically into the ventral thalamic region of the rat subjected to cardiac arrest cerebral ischemia (CACI). The delivery of the BDNF commenced 3 days before the CACI and lasted until the sacrifice of the animal at 7 days after cardiac arrest. Using specific monoclonal antibody for GABA demonstrated a striking proliferation and sprouting of GABA-ergic terminals in the ventral thalamic nucleus in the vicinity of the site of BDNF delivery. Also, there was a conspicious preservation of GABA-ergic neurons of the nucleus reticularis thalami on the side of BDNF application.