Barkai A I, Baron M, Kowalik S, Cooper T B
Psychiatry Res. 1986 Apr;17(4):261-7. doi: 10.1016/0165-1781(86)90073-9.
The inhibition by human plasma of 3H-imipramine (3H-IMI) specific binding to rat cerebral membranes was investigated using platelet-free plasma (PFP) from normal and depressed subjects. The specific binding of 3H-IMI at a ligand concentration of 4 nM decreased with increasing PFP volumes, reaching 50% inhibition following the addition of 10-13 microliters PFP to a final incubation volume of 250 microliters. The extent of this inhibition was the same using PFP from controls or depressed patients. The inhibitory activity was associated with plasma proteins. Scatchard analysis of 3H-IMI binding in the presence and absence of PFP indicated that the inhibitory effect was associated with an increased Kd without an appreciable change in Bmax. It is suggested that an endogenous acceptor in the PFP, such as alpha 1-acid-glycoprotein may be responsible for the observed inhibition of 3H-IMI binding to the cerebral membranes.
使用来自正常受试者和抑郁症患者的无血小板血浆（PFP），研究了人血浆对3H-丙咪嗪（3H-IMI）与大鼠脑膜特异性结合的抑制作用。在配体浓度为4 nM时，3H-IMI的特异性结合随着PFP体积的增加而降低，在向250微升的最终孵育体积中加入10 - 13微升PFP后达到50%抑制。使用来自对照组或抑郁症患者的PFP，这种抑制程度是相同的。抑制活性与血浆蛋白有关。对存在和不存在PFP时3H-IMI结合的Scatchard分析表明，抑制作用与Kd增加有关，而Bmax没有明显变化。有人提出，PFP中的内源性受体，如α1-酸性糖蛋白，可能是观察到的3H-IMI与脑膜结合受到抑制的原因。
