OBSERVATION ON BRAIN-DERIVED NEUROTROPHIC FACTOR IN CEREBRAL ISCHEMIA

我们的研究一般都集中在防御性和 可被激活以应对缺血的再生机制 损伤，以及这种潜在的治疗操作 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在增强型神经元发育中的作用 对缺血性损伤的抵抗，在诱导后3天表现出来 将抑郁扩散到大脑皮质。在治疗试验中，BDNF是 通过立体定向插入腹侧的微管给药 心脏骤停脑缺血大鼠丘脑区 (CACI)。BDNF的交付在CACI之前3天开始， 一直持续到动物心脏骤停后7天处死。 使用针对GABA的特异性单抗显示了惊人的 腹侧GABA能终末的增殖和发芽 脑源性神经营养因子投递部位附近的丘脑核团。另外， 核内GABA能神经元明显保存。 脑源性神经营养因子应用于丘脑网状核一侧。

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.