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 脑源性神经营养因子（BDNF）参与 发展增强的神经元对缺血性损伤的抗性， 在诱导扩散性抑制后3天， 皮层 在治疗试验中，BDNF通过 立体定向插入丘脑腹侧区的微管 脑缺血（CACI）大鼠心脏骤停模型。 的 BDNF的递送在CACI前3天开始，并持续到CACI结束。 在心脏骤停后7天处死动物。 使用特定 GABA的单克隆抗体显示了显著的增殖， 丘脑腹侧核GABA能终末的出芽 在BDNF传递位点附近。 还有一个显眼的 丘脑网状核GABA能神经元的保存 BDNF的应用。

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 brain-derived neurotrophic factor (BDNF) in the development of enhanced neuronal resistance to ischemic injury, demonstrable 3 days after induction of the spreading depression in the cortex. In therapeutic trials, BDNF was administered via the microcanullae 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 till the sacrifice of the animal at 7 days after cardiac arrest. Using specific monoclonal antibody for GABA demonstrated a striking proliferation and sprouting of GABAergic terminals in the ventral thalamic nucleus in the vicinity of the site of BDNF delivery. Also, there was a conspicuous preservation of GABAergic neurons of the nucleus reticularis thalami on the side of BDNF application.