强啡肽A（1－17）所致大鼠运动障碍及对脊髓组织AC－cAMP水平的影响

大鼠蛛网膜下腔注射强啡肽Ａ（１－１７），观察其所引起的行为变化及对脊髓组织ＡＣ－ｃＡＭＰ系统的影响。强啡肽Ａ（１－１７）５、１０、２０ｎｍｏｌ可引起大鼠双后肢弛缓性瘫痪，并在给药１０ｍｉｎ强啡肽Ａ（１－１７）１０、２０ｎｍｏｌ显著抑制脊髓组织ｃＡＭＰ含量和ＡＣ活性，呈量效关系，２ｈ后均有不同程度的恢复。选择性ｋ型阿片受体拮抗剂ｎｏｒ－ＢＮＩ３０ｎｍｏｌ可明显对抗强啡肽Ａ（１－１７）２０ｎｍｏｌ所致的后肢瘫痪并完全阻断其对ＡＣ、ｃＡＭＰ的抑制作用；Ｌ型Ｃａ２＋通道阻断剂异搏定１００ｎｍｏｌ亦可部分阻断强啡肽Ａ（１－１７）对脊髓的影响；而兴奋性氨基酸ＮＭＤＡ受体特异性拮抗剂ＡＰＶ１０ｎｍｏｌ则无效。提示ｋ型阿片受体和Ｌ型Ｃａ２＋通道参与了强啡肽Ａ（１－１７）所引起的大鼠运动障碍及对脊髓组织ＡＣ、ｃＡＭＰ水平的调控。

Dynorphin A(1-17) causes motor dysfunction and decreases adenylyl cyclase-cAMP level of spinal cord in rat

Influence of Dynorphin A(1-17)(Dyn)on motor function and adenylate cyclase(AC)-cAMP level after intrathecal injection (ith)were investigated .Dyn 5,10,20 nmol caused dose-dependent flaccid paralysis of hindlimbs.Dyn 10, 20 nmol decreased spinal adenylate cyclase(AC)activity andcyclic AMPproduction 10 min after ith.They recovered to varying extent two hours later.Pretreatment with selective k-opioid receptor antagonist nor-BNI 30 nmol 10 min before Dyn significantly blocked the effects of Dyn 20 nmol on hindlimb paralysis and inhibition of AC-cAMP level;L-type Ca2 channel blocker verapamil 100 nmol also played a role in blocking Dyn neurotoxicity while NMDA receptor antagonist APV 10 nmol had no effect.The results showed that k-opioid receptor and Ca2 channel play a role in spinal cord injury and regulation of AC-cAMP level by Dyn.