REGULATION OF HIPPOCAMPAL DYNORPHIN LEVELS AND SYNTHESIS AFTER ISCHEMIA

原位杂交研究表明， 在沙土鼠海马齿状回颗粒细胞中 缺血 通过以下谷物计数进行定量评估 放射自显影显示在24 h时减少约50% 再循环，与强啡肽的减少相当 在先前的研究中观察到的海马提取物中的免疫反应性。 强啡肽合成在转录水平上的下调， 与其他研究人员在癫痫发作后描述的情况相似， 与海马回路激活增加一致， 缺血 考虑到c-fos和hsp 70在此过程中的同时诱导， 细胞群，改变阿片肽前体的合成， 似乎是另一个组成部分， 神经元对局部缺血和其他疾病的复杂病理生理反应 压力

In situ hybridization studies demonstrate a decrease in prodynorphin mRNA in dentate granule cells of gerbil hippocampus following transient ischemia. Quantitative assessment by means of grain counts following autoradiography indicate a decrease of approximately 50% at 24h recirculation, comparable to the decreases in dynorphin peptide immunoreactivity in hippocampal extracts observed in previous studies. This down regulation of dynorphin synthesis at the transcriptional level is similar to that described by other investigators following seizures, and is consistent with an increased activation of hippocampal circuitry following ischemia. In view of the concurrent induction of c-fos and hsp7O in this cell population, altered synthesis of opioid peptide precursors would appear to be another component of what is coming to be understood as a complex pathophysiological response of neurons to ischemia and other stresses.