Department of Clinical Nutrition, Tang Du Hospital, the Fourth Military Medical University, Xi'an 710038, PR China.
Brain Res. 2011 Sep 9;1411:57-64. doi: 10.1016/j.brainres.2011.07.011. Epub 2011 Jul 12.
Previous research has demonstrated that diabetes induces learning and memory deficits. However, the mechanism of memory impairment induced by diabetes is poorly understood. The present study investigated the effect of streptozotocin (STZ)-induced diabetes on spatial learning and memory using the Morris Water Maze. The effects of diabetes on CA1 pyramidal neurons in hippocampus were also examined. Diabetes impaired spatial learning and memory of rats. Diabetes induced the apoptosis of neurons and translocation of Bax from cytoplasm to mitochondria. On the contrary, diabetes induced cytochrome c release into the cytoplasm from mitochondria. Release of Cyt-c from mitochondria into cytoplasm may play a role in apoptosis of the CA1 pyramidal neurons, which resulted in a decrease of the number of neurons in hippocampus and impaired the performance function. These results partially explain the mechanism of the effect of diabetes on learning and memory. To protect mitochondrial function is possible candidate for preventing the impairments of diabetes on hippocampal function.
先前的研究表明，糖尿病可导致学习和记忆功能障碍。然而，糖尿病引起记忆损伤的机制尚不清楚。本研究采用 Morris 水迷宫观察链脲佐菌素（STZ）诱导糖尿病对大鼠空间学习记忆能力的影响，并探讨其对海马 CA1 区锥体神经元的作用。糖尿病损害大鼠的空间学习记忆能力，诱导神经元凋亡和 Bax 从胞浆转位至线粒体。相反，糖尿病诱导细胞色素 C 从线粒体释放至胞浆。线粒体 Cyt-c 的释放可能在 CA1 区锥体神经元凋亡中起作用，导致海马神经元数量减少，学习记忆功能受损。这些结果部分解释了糖尿病对学习记忆功能影响的机制。保护线粒体功能可能是预防糖尿病对海马功能损伤的候选方法。
