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为探讨强啡肽（Ｄｙｎ）镇痛与致瘫的细胞机理，采用Ｆｕｒａ－２显微荧光光度技术观测了不同浓度的ＤｙｎＡ（１－１７）对原代培养脊髓神经元单个细胞内游离钙离子浓度（［Ｃａ２＋］ｉ）的影响．ＤｙｎＡ０．１－１００μｍｏｌ·Ｌ－１对基础［Ｃａ２＋］ｉ均无影响．ＤｙｎＡ０．１和１μｍｏｌ·Ｌ－１使高钾（５０ｍｍｏｌ·Ｌ－１）刺激的Ｃａ２＋内流峰值反应分别下降９４％（ｎ＝６）和８３％（ｎ＝４，Ｐ＜０．０５）；ＤｙｎＡ１０和１００μｍｏｌ·Ｌ－１对高钾刺激反应峰值无明显影响，但所有测试细胞均呈现持续性［Ｃａ２＋］ｉ升高；预先给予低浓度的ＤｙｎＡ（０．１和１μｍｏｌ·Ｌ－１），则高浓度ＤｙｎＡ（１０和１００μｍｏｌ·Ｌ－１）的促进作用明显减弱甚至消失．结果表明低浓度和高浓度ＤｙｎＡ（１－１７）对培养脊髓神经元的基础［Ｃａ２＋］ｉ无影响，但可分别抑制和促进去极化性钙离子内流，低浓度ＤｙｎＡ可对抗高浓度ＤｙｎＡ的促进作用．
To investigate the cellular mechanism of dynesophagealgia induced by dynorphin (Dyn), Fura-2 micro-fluorescence spectrophotometry was used to observe the effects of different concentrations of DynA (1-17) on intracellular free calcium Concentration ([Ca2 +] i). DynA0.1-100μmol·L-1 had no effect on basal [Ca2 +] i. DynA 0.1 and 1 μmol·L -1 decreased the Ca 2+ influx peak response by 50 mmol·L -1 by 94% (n = 6) and 83% (n = 4, P <0.05), respectively. DynA10 and 100μmol·L-1 had no significant effect on the peak of high-potassium stimulation, but all the test cells showed persistent increase of [Ca2 +] i. Pretreatment with low concentrations of DynA (0.1 and 1μmol·L-1) The promotion effect of high concentrations of DynA (10 and 100μmol·L-1) significantly reduced or even disappeared. The results showed that low concentration and high concentration of DynA (1-17) had no effect on the basic [Ca2 +] i of cultured spinal cord neurons, but inhibited and promoted the influx of depolarizing calcium ions respectively. Low concentration of DynA could antagonize the high concentration of DynA The promotion effect.