Kilpatrick G J, Butler A, Hagan R M, Jones B J, Tyers M B
Department of Neuropharmacology, Glaxo Group Research Ltd., Ware, Herts, UK.
Naunyn Schmiedebergs Arch Pharmacol. 1990 Jul;342(1):22-30. doi: 10.1007/BF00178967.
GR67330 potently inhibited 5-hydroxytryptamine (5-HT)-induced depolarizations of the rat isolated vagus nerve. At the higher concentrations used (0.3 nmol/l-1 nmol/l) this was accompanied by a marked reduction in the maximum response to 5-HT. The calculated pKB value was 10.2. The binding of the tritiated derivative of GR67330 to homogenates of rat entorhinal cortex was examined. Kinetic analysis revealed that specific [3H] GR67330 (0.1 nmol/l) binding was rapid and reversible. Association and dissociation rate constants were 1.48 +/- 0.36 x 10(8) mol/l-1 s-1 and 7.85 +/- 0.41 x 10(-3) s-1 respectively. Equilibrium saturation analysis revealed specific binding was to a single site (Bmax 22.6 +/- 0.21 fmol/mg protein) of high affinity (Kd 0.038 +/- 0.003 nmol/l). At low ligand concentrations, specific binding was up to 90% of total binding. If unlabelled GR67330 was used to define non-specific binding two sites were evident (Kd1 0.066 +/- 0.007 nmol/l, Kd2 20.1 +/- 9.7 nmol/l; Bmax1 31.5 +/- 3.2 fmol/mg protein, Bmax2 1110 +/- 420 fmol/mg protein). [3H] GR67330 binding was inhibited potently by 5-HT3 antagonists and agonists. Ligands for other 5-HT receptors and other neurotransmitter receptors were either only weakly active or inactive at inhibiting binding. Hill numbers for antagonist inhibition of binding were close to unity, except for quipazine which was significantly greater than one. In common with other 5-HT3 binding studies, all 5-H-agonist tested had Hill numbers greater than one (1.51-1.71). GR38032 and GR65630 inhibited a greater proportion of binding than other 5-HT3 antagonists, this additional binding was interpreted as inhibition from a second saturable site unrelated to the 5-HT3 receptor.(ABSTRACT TRUNCATED AT 250 WORDS)
GR67330能有效抑制5-羟色胺(5-HT)诱导的大鼠离体迷走神经去极化。在使用的较高浓度(0.3纳摩尔/升 - 1纳摩尔/升)下,这伴随着对5-HT最大反应的显著降低。计算得出的pKB值为10.2。研究了GR67330的氚化衍生物与大鼠内嗅皮质匀浆的结合情况。动力学分析表明,特异性[3H]GR67330(0.1纳摩尔/升)结合迅速且可逆。结合和解离速率常数分别为1.48±0.36×10(8)摩尔/升-1·秒-1和7.85±0.41×10(-3)秒-1。平衡饱和分析表明,特异性结合是到一个高亲和力的单一位点(Bmax为22.6±0.21飞摩尔/毫克蛋白)(Kd为0.038±0.003纳摩尔/升)。在低配体浓度下,特异性结合高达总结合的90%。如果用未标记的GR67330来定义非特异性结合,则有两个位点明显(Kd1为0.066±0.007纳摩尔/升,Kd2为20.1±9.7纳摩尔/升;Bmax1为31.5±3.2飞摩尔/毫克蛋白,Bmax2为1110±420飞摩尔/毫克蛋白)。[3H]GR67330结合被5-HT3拮抗剂和激动剂强烈抑制。其他5-HT受体和其他神经递质受体的配体在抑制结合方面要么活性很弱,要么无活性。除了喹哌嗪的希尔系数明显大于1外,拮抗剂抑制结合的希尔系数接近1。与其他5-HT3结合研究一样,所有测试的5-HT激动剂的希尔系数都大于1(1.51 - 1.71)。GR38032和GR65630比其他5-HT3拮抗剂抑制的结合比例更大,这种额外的结合被解释为来自与5-HT3受体无关的第二个可饱和位点的抑制作用。(摘要截断于250字)