Wojcik W J, Ulivi M, Paez X, Costa E
Fidia Georgetown Institute for the Neurosciences, Georgetown University School of Medicine, Washington D.C. 20007.
J Neurochem. 1989 Sep;53(3):753-8. doi: 10.1111/j.1471-4159.1989.tb11769.x.
gamma-Aminobutyric acidB (GABAB) receptor recognition sites that inhibit cyclic AMP formation, open potassium channels, and close calcium channels are coupled to these effector systems by guanine nucleotide binding proteins (G proteins). These G proteins are ADP-ribosylated by islet-activating protein (IAP), also known as pertussis toxin. This process prevents receptor coupling to these G proteins. In slices of cerebral cortex and hippocampus from rat, stimulation of GABAB receptors with baclofen, a receptor agonist, also potentiates the accumulation of cyclic AMP stimulated by beta-adrenergic agonists. It was unknown whether those GABAB receptors that potentiate the beta-adrenergic response were also sensitive to IAP. IAP was injected intracerebroventricularly into rats to ADP-ribosylate IAP-sensitive G proteins. Four days after the IAP injection, 38% and 52% of these G proteins from cerebral cortex and hippocampus, respectively, were ADP-ribosylated by the IAP injection. In slices of both structures prepared from IAP-treated rats, the GABAB receptor-mediated potentiation of the beta-adrenergic receptor response was attenuated. Thus, many GABAB receptor-mediated responses are coupled to IAP-sensitive G proteins.
抑制环磷酸腺苷（cAMP）形成、开放钾通道并关闭钙通道的γ-氨基丁酸B（GABAB）受体识别位点，通过鸟嘌呤核苷酸结合蛋白（G蛋白）与这些效应系统偶联。这些G蛋白被胰岛激活蛋白（IAP）（也称为百日咳毒素）进行ADP核糖基化。这一过程会阻止受体与这些G蛋白偶联。在大鼠大脑皮层和海马体切片中，用受体激动剂巴氯芬刺激GABAB受体，也会增强β-肾上腺素能激动剂刺激的环磷酸腺苷的积累。增强β-肾上腺素能反应的那些GABAB受体是否也对IAP敏感尚不清楚。将IAP脑室内注射到大鼠体内，以使对IAP敏感的G蛋白进行ADP核糖基化。IAP注射4天后，来自大脑皮层和海马体的这些G蛋白分别有38%和52%被IAP注射进行了ADP核糖基化。在由IAP处理过的大鼠制备的这两种结构的切片中，GABAB受体介导的β-肾上腺素能受体反应的增强作用减弱。因此，许多GABAB受体介导的反应与对IAP敏感的G蛋白偶联。
