DeHaven-Hudkins D L, Fleissner L C
Department of Enzymology and Receptor Biochemistry, Sterling Winthrop Pharmaceuticals Research Division, Malvern, PA 19355-1314.
Life Sci. 1992;50(9):PL65-70. doi: 10.1016/0024-3205(92)90255-n.
In saturation binding experiments, (+)pentazocine, (+)3-(3-hydroxyphenyl)-N-propylpiperidine (3-PPP), haloperidol and rimcazole did not inhibit the binding of [3H]DTG in a purely competitive fashion. Although Scatchard analysis indicated that [3H]DTG bound to a single site, the inhibition curves of some, but not all, reference compounds exhibited Hill coefficients of less than 0.8. The Scatchard data were consistent with a model of hyperbolic competitive inhibition of binding to the [3H]DTG-defined sigma site, although other possibilities such as negative cooperativity or binding to two sites cannot be definitively excluded. Compounds from numerous pharmacological and structural classes inhibited the binding of [3H]DTG, suggesting that interactions of [3H]DTG with other receptors may have confounded the Scatchard analysis of the binding of [3H]DTG to sigma recognition sites.
在饱和结合实验中，（+）喷他佐辛、（+）3-（3-羟基苯基）-N-丙基哌啶（3-PPP）、氟哌啶醇和利咪唑并非以纯粹竞争性方式抑制[3H]DTG的结合。尽管Scatchard分析表明[3H]DTG结合于单一位点，但部分（而非全部）参考化合物的抑制曲线显示希尔系数小于0.8。Scatchard数据与结合至[3H]DTG定义的σ位点的双曲线竞争性抑制模型相符，不过诸如负协同性或结合至两个位点等其他可能性也不能被完全排除。来自众多药理学和结构类别的化合物抑制了[3H]DTG的结合，这表明[3H]DTG与其他受体的相互作用可能干扰了对[3H]DTG与σ识别位点结合的Scatchard分析。
