Chavkin C, Bloom F E
Neuropeptides. 1986 Jan;7(1):19-22. doi: 10.1016/0143-4179(86)90074-0.
The opioid receptor antagonists, naloxone and beta-chlornaltrexamine, were used to determine whether activation of endogenous opioid peptide containing pathways produced pharmacologically reversible opioid actions. Extracellularly recorded responses of the hippocampal CA3 pyramidal cells were evoked by stimulation of the dynorphin-containing mossy fiber pathway. Neither naloxone nor beta-chlornaltrexamine pretreatment significantly changed the evoked response. However, both antagonists blocked the effect of applied dynorphin-A(1-17) on CA1 pyramidal cell evoked responses. Thus, our data demonstrate that if endogenous opioids are released from this pathway, the peptides cannot be responsible for the evoked response measured in hippocampal CA3 cellular field. With no direct evidence for endogenous opioid peptides acting through opioid receptors, the neurotransmitter role of dynorphins in rat hippocampus remains obscure.
阿片受体拮抗剂纳洛酮和β-氯诺美沙明被用于确定含内源性阿片肽通路的激活是否会产生药理学上可逆的阿片样作用。通过刺激含强啡肽的苔藓纤维通路诱发海马CA3锥体细胞的细胞外记录反应。纳洛酮和β-氯诺美沙明预处理均未显著改变诱发反应。然而，两种拮抗剂均阻断了施加的强啡肽A（1-17）对CA1锥体细胞诱发反应的影响。因此，我们的数据表明，如果内源性阿片类物质从该通路释放，这些肽不可能是在海马CA3细胞区域测量到的诱发反应的原因。由于没有直接证据表明内源性阿片肽通过阿片受体起作用，强啡肽在大鼠海马中的神经递质作用仍不清楚。
