Zawilska J, Lajtha A, Borsodi A
Institute of Biochemistry, Biological Research Center of the Hungarian Academy of Sciences, Szeged.
J Neurochem. 1988 Sep;51(3):736-9. doi: 10.1111/j.1471-4159.1988.tb01806.x.
Selective binding of [3H]bremazocine and [3H]-ethylketocyclazocine to kappa-opioid receptor sites in frog (Rana esculenta) brain membranes is irreversibly inactivated by the sulfhydryl group alkylating agent N-ethylmaleimide (NEM). Pretreatment of the membranes with kappa-selective compounds [ethylketocyclazocine (EKC), dynorphin (1-13), or U-50,488H] but not with [D-Ala2,N-Me-Phe4,Gly5-ol]enkephalin (DAGO; mu specific ligand) or [D-Ala2,N-Me-Phe4,Gly5-ol]enkephalin (DADLE; delta specific ligand) strongly protects the binding of the radioligands against NEM inactivation. These results provide more evidence for the existence of kappa-opioid receptors in frog brain. The relatively high concentrations of NEM that are needed to decrease the specific binding of [3H]bremazocine together with the observation of an almost complete protection of its binding sites by NaCl suggest that bremazocine may act as an opioid antagonist in frog brain.
[3H]布瑞马佐辛和[3H] - 乙基酮环唑辛与青蛙（食用蛙）脑膜中κ-阿片受体位点的选择性结合可被巯基烷基化剂N - 乙基马来酰亚胺（NEM）不可逆地灭活。用κ-选择性化合物[乙基酮环唑辛（EKC）、强啡肽（1 - 13）或U - 50,488H]预处理脑膜，但不用[D - Ala2，N - Me - Phe4，Gly5 - ol]脑啡肽（DAGO；μ特异性配体）或[D - Ala2，N - Me - Phe4，Gly5 - ol]脑啡肽（DADLE；δ特异性配体）预处理，能强烈保护放射性配体的结合免受NEM灭活。这些结果为青蛙脑中存在κ-阿片受体提供了更多证据。降低[3H]布瑞马佐辛特异性结合所需的相对高浓度的NEM，以及NaCl对其结合位点几乎完全保护的观察结果表明，布瑞马佐辛在青蛙脑中可能作为阿片拮抗剂起作用。
