Chavkin C, Henriksen S J, Siggins G R, Bloom F E
Brain Res. 1985 Apr 8;331(2):366-70. doi: 10.1016/0006-8993(85)91565-3.
Dynorphin-A1-17 and dynorphin-B increased the evoked response of hippocampal CA1 pyramidal cells, as did other opioids tested. Treatment of the hippocampal slice with beta-funaltrexamine, a mu-receptor selective antagonist, blocked the effects of normorphine, dynorphin-A and dynorphin-B, but did not change the response to D-Ala2, D-Leu5-enkephalin. The low potency of kappa selective agonists and the antagonism by beta-funaltrexamine of the dynorphins' effect indicate that kappa-opioid receptors may not be involved in these observed responses. Our data suggest that both mu- and delta-receptors are functionally represented and provide evidence that the dynorphins or their derivatives may also be agonists at the mu-receptor.
强啡肽 A1-17 和强啡肽 B 增强了海马 CA1 锥体神经元的诱发反应，其他受试阿片类药物也有此作用。用 μ 受体选择性拮抗剂β-芬基曲马多处理海马脑片，可阻断去甲吗啡、强啡肽 A 和强啡肽 B 的作用，但不改变对 D-丙氨酸 2、D-亮氨酸 5-脑啡肽的反应。κ 选择性激动剂的低效性以及β-芬基曲马多对强啡肽作用的拮抗表明，κ 阿片受体可能不参与这些观察到的反应。我们的数据表明，μ 受体和δ受体在功能上均有体现，并提供证据表明强啡肽或其衍生物也可能是μ受体的激动剂。
