Cholecystokinin-8 suppressed 3H-etorphine binding to rat brain opiate receptors.
Cholecystokinin-8 suppressed 3H-etorphine binding to rat brain opiate receptors.
复制标题
DOI：
10.1016/0024-3205(89)90285-3
复制
发表时间：
1989
期刊：
影响因子：
6.1
通讯作者：
X. J. Wang;S. Fan;M. Ren;J. Han
中科院分区：
文献类型：
--
作者：
X. J. Wang;S. Fan;M. Ren;J. Han
用放射受体分析法（RRA）研究了CCK-8对~ 3 H-埃托啡与大鼠脑突触体膜（P_2）阿片受体结合的影响。在竞争实验中，CCK-8（1 pM ~ 1 μM）抑制~ 3 H-埃托啡的结合。1 μM丙谷胺可完全逆转该效应。Rosenthal饱和度分析显示两个群体的3 H-埃托啡结合位点。CCK-8（1 pM至1μM）通过增加Kd（高达+235%）和降低Bmax（高达-80%）抑制3 H-埃托啡与高亲和力位点的结合，而对低亲和力位点的Kd和Bmax没有显著影响。CCK-8（10 nM）的这种作用也可被1 μM丙谷胺完全逆转。未硫酸化CCK-8（100 pM至1 μM）仅使高亲和力位点的Kd略微增加（+64%），而不影响Bmax。结果提示CCK-8可能通过激活CCK受体而抑制高亲和力阿片结合位点。
Radio receptor assay (RRA) was adopted to analyse the influence of CCK-8 on 3H-etorphine binding to opiate receptors in rat brain synaptosomal membranes (P2). In the competition experiment CCK-8 (1pM to 1 μM) suppressed the binding of3H-etorphine. This effect was completely reversed by proglumide at 1 μM. Rosenthal analysis for saturation revealed two populations of3H-etorphine binding sites. CCK-8 (1pM to 1μM) inhibited3H-etorphine binding to the high affinity sites by an increase in Kd (up to +235%) and decrease in Bmax (up to −80%) without significant changes in the Kd and Bmax of the low affinity sites. This effect of CCK-8 (10nM) was also completely reversed by proglumide at 1 μM. Unsulfated CCK-8 (100pM to 1 μM) produced only a slight increase in Kd of the high affinity sites (+64%) without affecting Bmax. The results suggest that CCK-8 might be capable of suppressing the high affinity opioid binding sites via the activation of CCK receptor.