Li X M, Jansson A, Finnman U B, Agnati L F, Fuxe K
Department of Neuroscience, Karolinska Institute, Stockholm, Sweden.
Neurosci Lett. 1997 Jun 13;228(3):171-4. doi: 10.1016/s0304-3940(97)00392-3.
A G(i)-protein antibody AS/7 at 1:10 dilution significantly increased the K(d) values of the D2 agonist [3H]N-propylnorapomorphine (NPA) binding sites in the rat striatal membranes, and coincubation with sulphated cholecystokinin octapeptide (CCK-8; 1 nM) did not further increase the K(d) values. A GTP analogue guanylyl-imidodiphosphate (GMP-PNP) at 100 microM markedly increased the K(d) values of the [3H]NPA binding sites in the rat forebrain sections, and coincubation with CCK-8 (1 nM) again did not produce a further increase in the K(d) values. The present results indicate that abnormal activity of G-proteins abolished the ability of CCK-8 to reduce the D2 receptor affinity in the brain.
稀释至1:10的G(i)蛋白抗体AS/7显著增加了大鼠纹状体膜中D2激动剂[3H]N-丙基去甲阿朴吗啡（NPA）结合位点的解离常数（K(d)值），与硫酸化八肽胆囊收缩素（CCK-8；1 nM）共同孵育并未进一步增加K(d)值。100 μM的鸟苷酸类似物鸟苷酰亚胺二磷酸（GMP-PNP）显著增加了大鼠前脑切片中[3H]NPA结合位点的K(d)值，与CCK-8（1 nM）共同孵育同样未使K(d)值进一步增加。目前的结果表明，G蛋白的异常活性消除了CCK-8降低脑中D2受体亲和力的能力。
