REGULATION OF HIPPOCAMPAL DYNORPHIN LEVELS AND SYNTHESIS AFTER ISCHEMIA

早期的研究结果显示，海马区持续耗尽。 沙土鼠脑缺血后强啡肽的表达。小鼠的免疫反应性 海马体提取物至少在50%的对照水平上保持不变 单次5分钟缺血发作后一周。免疫细胞化学 研究证实强啡肽在脑内的定位 海马齿状颗粒细胞及其苔藓纤维投射 转到CA3。免疫反应模式保持不变 短暂性脑缺血后再循环，提示 脑缺血后强啡肽的耗竭是 在整个细胞群体中都是同质的。未来的研究将 目的：探讨前强啡肽原在脑内的表达及分布。 缺血后的海马区。

Earlier results had demonstrated a lasting depletion of hippocampal dynorphin after ischemia in the gerbil. Immunoreactivity in hippocampal extracts remained at 50% of control levels for at least one week after a single 5 min ischemic episode. Immunocytochemical studies verify the localization of dynorphin peptides in hippocampal dentate granule cells an their mossy fiber projections to CA3. The pattern of immunoreactivity remains unchanged during recirculation after transient ischemia, suggesting that the postischemic depletion of dynorphin peptides is homogeneous throughout this cell population. Future studies will evaluate the levels and distribution of prodynorphin mRNA in hippocampus after ischemia.