Cholecystokinin-8 suppressed 3H-etorphine binding to rat brain opiate receptors.
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 microM) suppressed the binding of 3H-etorphine. This effect was completely reversed by proglumide at 1 microM. Rosenthal analysis for saturation revealed two populations of 3H-etorphine binding sites. CCK-8 (1pM to 1 microM) inhibited 3H-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 microM. Unsulfated CCK-8 (100pM to 1 microM) 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.
Wang
X J
XJ
Department of Physiology, Beijing Medical University, China.
Fan
S G
SG
Ren
M F
MF
Han
J S
JS
D000818:Animals; D001667:Binding, Competitive; D001921:Brain / Q000378:metabolism*; D005048:Etorphine / Q000378:metabolism*; D009019:Morphinans / Q000378:metabolism*; D051381:Rats; D011957:Receptors, Opioid / Q000378:metabolism*; D012844:Sincalide / Q000494:pharmacology*; D014316:Tritium
D009019:Morphinans; D011957:Receptors, Opioid; D014316:Tritium; D005048:Etorphine; D012844:Sincalide