Sánchez-Blázquez P, Garzón J
Instituto Cajal, CSIC, Madrid, Spain.
Eur J Pharmacol. 1994 Jun 2;258(1-2):159-62. doi: 10.1016/0014-2999(94)90070-1.
Intracerebroventricular (i.c.v.) administration of the venom peptide, mastoparan, to mice decreased to a limited extent opioid-induced supraspinal analgesia in a non-competitive fashion. The mu-opioid receptor agonists, [D-Ala2,N-MePhe4,Gly-ol5]-enkephalin (DAMGO) and morphine, the mu/delta-opioid receptor ligands, human beta-endorphin-(1-31) and [D-Ala2,D-Leu5]-enkephalin (DADLE), and the selective ligands of delta-opioid receptors, [D-Pen2,5]enkephalin (DPDPE) and [D-Ala2]deltorphin II, showed an impaired analgesic effect in mice given mastoparan. Mastoparan diminished the analgesic activity of DPDPE and [D-Ala2]deltorphin II to the same extent as observed after giving the delta-opioid receptor-selective antagonist, ICI 174864. The mu-opioid receptor-mediated analgesia that remained after mastoparan was abolished in the presence of the opioid antagonist, naloxone. Mastoparan after binding to Gi alpha/Go alpha subunits could block opioid antinociception. The existence of a class of G protein functionally coupled to mu-opioid receptors, but resistant to the effect of mastoparan is suggested.
向小鼠脑室内（i.c.v.）注射毒液肽mastoparan，以非竞争性方式在一定程度上降低了阿片类药物诱导的脊髓上镇痛作用。μ-阿片受体激动剂[D-Ala2，N-MePhe4，Gly-ol5]-脑啡肽（DAMGO）和吗啡、μ/δ-阿片受体配体人β-内啡肽-（1-31）和[D-Ala2，D-Leu5]-脑啡肽（DADLE），以及δ-阿片受体的选择性配体[D-Pen2,5]脑啡肽（DPDPE）和[D-Ala2]强啡肽II，在给予mastoparan的小鼠中显示出镇痛作用受损。Mastoparan降低DPDPE和[D-Ala2]强啡肽II的镇痛活性的程度与给予δ-阿片受体选择性拮抗剂ICI 174864后观察到的程度相同。在阿片受体拮抗剂纳洛酮存在的情况下，mastoparan后残留的μ-阿片受体介导的镇痛作用被消除。Mastoparan与Giα/Goα亚基结合后可阻断阿片类药物的抗伤害感受作用。提示存在一类与μ-阿片受体功能偶联但对mastoparan的作用具有抗性的G蛋白。
