Elucidation of the mechanisms of the impairment of functional neuron networks and establishment of the therapeutic strategies.

1. 抗过敏药物如氨lexanox、色胺酸等与S-100、视蛋白样蛋白14-3-3结合，抑制其功能。在大鼠脑发育过程中，细胞周期蛋白依赖性激酶5 （cyclin-dependent kinase 5, Cdk5）的表达水平未发生变化，其激活因子p35的表达水平发生了变化。钙调素依赖性蛋白激酶（CaMK） I和IV参与了大鼠海马切片长期增强的形成。一种新的钙结合蛋白calbrain抑制CaMK ii。使用一种钙调神经磷酸酶特异性抑制剂FK506，钙调神经磷酸酶被证明参与了点燃大鼠的癫痫发生。通过对衰老加速小鼠（SAM）的研究，发现血脑屏障的损伤发生在衰老过程中。低温处理对脑缺血后迟发性神经元死亡有保护作用。在治疗后，尽可能慢地将体温升高到正常水平是很重要的。胎儿海马细胞神经元移植诱导记忆和学习障碍大鼠的恢复。免疫抑制药物（FK506和环孢素A）抑制钙调磷酸酶，促进生长激素的转录和翻译。

1. Anti-allergic drugs such as amlexanox and cromolyn bound to S-100, visin-like protein, and 14-3-3, and inhibited their functions.2. During the developmental processes of rat brain, the expression level of cyclin-dependent kinase 5 (Cdk5) did not alter, and its activaot, p35, did.3. Calmodulin-dependent protein kinases (CaMK) I and IV were involved in the formation of long-term potentiation using rat hippocampal slices. A novel calcium-binding protein, calbrain, inhibited CaMK II.4. Using a calcineurin-specific inhibitor, FK506, calcineurin was shown to be involved in the epileptogenesis of the kindled rats.5. By the study using SAM (Senescence-Accelerated Mouse), the impairment of blood-brain barrier was shown to occur during the aging processes.6. The hypothermic treatment worked effectively to protect the delayed neuronal death after the brain ischemia. It was important to raise the body temperature to the normal level as slow as possible after this therapy.7. Neuronal transplantation of fetal hippocampal cells induced the recovery of the memory and learning impaired rats.8. Transcription and translation of growth hormone was enhanced by the inhibition of calcineurin using immunosuppressive drugs (FK506 and cyclosporin A).