Zhang K M, Wang X M, Mokha S S
Department of Physiology, Meharry Medical College, Nashville, TN 37208, USA.
Brain Res. 1996 May 6;719(1-2):229-33. doi: 10.1016/0006-8993(96)00123-0.
Extracellular single unit recordings were made from 74 neurons in the superficial and deeper dorsal horn of the medulla (trigeminal nucleus caudalis). N-methyl-D-aspartic acid (NMDA) excited nociceptive as well as non-nociceptive neurons. NMDA receptor antagonist, DL-2-Amino-5-Phosphonovaleric acid (AP-5), blocked the NMDA-evoked excitation. Microiontophoretic application of a selective mu-opioid receptor agonist, [D-Ala2,N-Me-Phe4,Gly5-ol]enkephalin (DAMGO), reduced the NMDA-evoked responses of 100% of nociceptive specific (NS), 93% of wide dynamic range (WDR) and 86% of low threshold (LT) neurons in the superficial and deeper dorsal horn of the medulla. In contrast, application of a selective delta 1-opioid receptor agonist, [D-Pen2,5]enkephalin (DPDPE), reduced the NMDA-evoked responses of 90% of NS neurons, 72% of WDR neurons and 67% of LT neurons in the superficial and deeper dorsal horn of the medulla. DPDPE also produced excitatory or biphasic effects. The inhibitory actions of DAMGO and DPDPE were reversed by naloxone and/or 7-benzylidenenaltrexone (BNTX), mu- and delta 1-receptor antagonists. It is concluded that mu- and delta-opioid receptor agonists produce a predominantly inhibitory modulation of the NMDA-evoked responses of nociceptive and non-nociceptive neurons in the medullary dorsal horn.
在延髓（三叉神经尾侧核）浅层和深层背角的74个神经元上进行了细胞外单单位记录。N-甲基-D-天冬氨酸（NMDA）可兴奋伤害性神经元和非伤害性神经元。NMDA受体拮抗剂DL-2-氨基-5-磷酸缬氨酸（AP-5）可阻断NMDA诱发的兴奋。通过微量离子电泳施加选择性μ阿片受体激动剂[D-Ala2，N-Me-Phe4，Gly5-ol]脑啡肽（DAMGO），可降低延髓浅层和深层背角中100%的伤害性特异性（NS）神经元、93%的广动力范围（WDR）神经元和86%的低阈值（LT）神经元对NMDA诱发的反应。相比之下，施加选择性δ1阿片受体激动剂[D-Pen2，5]脑啡肽（DPDPE），可降低延髓浅层和深层背角中90%的NS神经元、72%的WDR神经元和67%的LT神经元对NMDA诱发的反应。DPDPE还产生兴奋或双相作用。DAMGO和DPDPE的抑制作用可被μ和δ1受体拮抗剂纳洛酮和/或7-苄叉基纳曲酮（BNTX）逆转。得出的结论是，μ和δ阿片受体激动剂对延髓背角中伤害性和非伤害性神经元的NMDA诱发反应产生主要的抑制性调节作用。
