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蛛网膜下腔注射（ｉ．ｔ．）强啡肽Ａ１－１７（Ｄｙｎ）引起剂量依赖性后肢和尾部瘫痪及甩尾甩足抑制。脊髓背角（侧）ＮＭＤＡ受体和ＮＯＳ／ＮＯ功能活性下降可能与Ｄｙｎ镇痛作用有关，脊髓腹角（侧）ＮＭＤＡ受体－Ｃａ２＋－ＮＯＳ／ＮＯ通路过度激活及ｃ－ｆｏｓ高表达可能与Ｄｙｎ致脊髓损伤（ＳＣＩ）作用有关。在Ｄｙｎ致ＳＣＩ机制中，过量ＮＯ（细胞水平）具有神经毒性作用，脑源性ＮＯＳ主要在早期，诱生型ＮＯＳ主要在后期起作用，而内皮细胞源性ＮＯＳ和适量ＮＯ（血管水平）可能具有保护作用。在原代培养脊髓神经元中，高浓度Ｄｙｎ可通过ＮＭＤＡ受体和κ受体直接引起细胞内Ｃａ２＋超负荷，低浓度Ｄｙｎ只通过κ受体抑制高钾刺激性Ｃａ２＋内流
Subarachnoid injections (i.t.) Dynorphin A1-17 (Dyn) caused a dose-dependent inhibition of paraplegia and tail flick in the hindlimb and tail. The decreased spinal cord dorsal horn (NMDA) receptor and NOS / NO functional activity may be related to the analgesic effect of Dyn. The over-activation of the NMDA receptor-Ca2 + -NOS / NO pathway and the high c-fos expression in the ventral horn (lateral) Dyn caused by the role of spinal cord injury (SCI). In the SCI induced by Dyn, excessive NO (neuronal toxicity) is neurotoxic. Brain-derived NOS is mainly in the early stage. Inducible NOS mainly plays a role in the later stage. Endothelial cell-derived NOS and proper NO (blood vessel level) Has a protective effect. In primary cultured spinal cord neurons, high concentration of Dyn can directly cause intracellular Ca2 + overload through NMDA receptor and κ receptor, while low concentration of Dyn can inhibit high potassium-stimulated Ca2 + influx through κ receptor