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本实验观察了CCK—8对[~3H]Et与大鼠脑阿片受体结合的影响.含硫CCK—8能抑制[~3H]Et与高亲和位点的结合,使K_D值增大(P<0.001),B_(max)减小(P<0.01),在10 fmol/L～Lμmol/L范围内呈量效关系.但对低亲和位点的结合没有影响.无硫CCK—8仅对[~3H]Et高亲和位点的K_D值有较小程度的增大(P<0.05),不影响B_(max)值.CCK—8(10 nmol/L)抑制[~3H]Et与阿片受体结合的作用能被CCK受体拮抗剂谷丙酰胺(1μmol/L)所阻断.结果提示,CCK—8可能通过激活CCK受体发挥对阿片受体的抑制作用。
The effect of CCK-8 on the binding of [~ 3H] Et to rat opioid receptors was observed in this experiment.Condensation of [~ 3H] Et with high affinity sites by sulfur-containing CCK-8 increased the K_D value (P <0.001), B max (P <0.01), and the dose-effect relationship was in the range of 10 fmol / L to Lμmol / L, but had no effect on the binding of low affinity sites. 8 only had a small increase in the value of K_D at [~ 3H] Et high affinity sites (P <0.05), but did not affect the value of B max.CCK-8 (10 nmol / L) inhibited [~ 3H ] Et and opioid receptor can be blocked by the CCK receptor antagonist glutamate (1μmol / L) .The results suggest that CCK-8 may exert opioid receptor inhibition by activating CCK receptor.