REGULATION OF HIPPOCAMPAL DYNORPHIN LEVELS AND SYNTHESIS AFTER ISCHEMIA

来自每种内源性阿片前体的多肽 在短暂性脑缺血后的沙土鼠脑区进行检测。 观察强啡肽A免疫反应性的持续耗竭 只有在海马区。海马区强啡肽水平下降了30%- 40%早在再循环后1小时，并保持在50% 控制至少一周。在一些实验中，多肽水平 24小时后出现一过性恢复。初步结果表明 海马区强啡肽原基因表达水平也有类似的降低 有着相似的时间进程。 这些结果在神经化学水平上证明了一种独特的 含强啡肽齿状颗粒剂的敏感性研究 细胞/苔藓纤维通路通向短暂性脑缺血。尽管这些 细胞在组织上保持完好，强啡肽的减少 在延迟性海马区丧失之前和期间继续 CA1神经元的特征，并进一步定义了 海马区回路的选择性易损性 缺血症。多肽耗竭的机制，以及 强啡肽在生理和生理功能中的作用 海马体的病理机制仍有待阐明。

Peptides derived from each of the endogenous opioid precursors were measured in gerbil brain regions after transient ischemia. Lasting depletion of dynorphin A immunoreactivity were observed only in hippocampus. Levels of hippocampal dynorphin fell by 30- 40% as early as 1 hr after recirculation and remained at 50% of control for at least one week. In some experiments peptide levels showed a transient recovery at 24 hr. Preliminary results suggest a similar reduction in hippocampal pro-dynorphin mRNA levels with a similar time course. These results demonstrate at the neurochemical level a unique sensititivity of the dynorphin-containing dentate granule cell/mossy fiber pathway to transient ischemia. Although these cells remain histologically intact, the decrease in dynorphin precedes and continues during the delayed loss of hippocampal CA1 neurons characteristic of this model and further defines the selective vulnerability of hippocampal circuitry following ischemia. The mechanisms responsible for peptide depletion, and the functional roles of dynorphin peptides in the physiology and pathology of the hippocampus, remain to be elucidated.