Decrease in [3H]-serotonin binding in rat brain produced by the repeated administration of either monoamine oxidase inhibitors or centrally acting serotonin agonists.
Decrease in [3H]-serotonin binding in rat brain produced by the repeated administration of either monoamine oxidase inhibitors or centrally acting serotonin agonists.
复制标题
重复施用单胺氧化酶抑制剂或中枢作用的血清素激动剂会导致大鼠脑中[3H]-血清素结合减少。
DOI：
10.1016/0028-3908(80)90102-1
复制
发表时间：
1980
影响因子：
4.7
通讯作者：
Frazer,A
中科院分区：
文献类型：
--
作者：
Savage,DD;Mendels,J;Frazer,A
研究了重复施用单胺氧化酶抑制剂或血清素激动剂对大鼠大脑皮层中[3H]-血清素结合和血清素浓度的影响。仅给予五天的氯吉林就会导致[3H]-血清素结合显着减少，但在用消耗脑血清素的药物预处理的动物中却无法做到这一点。用α-甲基-甲状酪氨酸预处理大鼠并不能阻止氯吉林诱导的[3H]-血清素结合减少。用尼亚酰胺重复治疗大鼠也降低了[3H]-血清素结合，并且结合位点恢复到对照值与血清素浓度恢复到对照值在时间上相关。向大鼠重复施用血清素激动剂、喹嗪或 TFMPP，导致[3H]-血清素结合减少。氯吉林和血清素激动剂诱导的[3H]-血清素结合减少是由于最大特异性结合能力显着降低，而表观结合常数没有变化。这里提供的数据与 MAO 抑制剂通过随时间增加血清素受体对吲哚烷基胺的暴露而间接减少 [3H]-血清素结合的假设是一致的。
The effect of repeated administration of monoamine oxidase inhibitors or serotonin agonists on [3H]-serotonin binding and serotonin concentrations in rat cerebral cortex was examined. Five days of clorgyline administration, which alone caused a significant reduction in [3H]-serotonin binding, was unable to do this in animals pretreated with drugs that deplete brain serotonin. Pretreatment of rats with alpha-methyl-paratyrosine did not block the clorgyline-induced reduction in [3H]-serotonin binding. Repeated treatment of rats with nialamide also lowered [3H]-serotonin binding and the return of binding sites to control values was correlated temporally with the return of the serotonin concentration to control values. Repeated administration to rats of the serotonin agonists, quipazine or TFMPP, produced a decrease in [3H]-serotonin binding. Both the clorgyline and serotonin agonist-induced reduction in [3H]-serotonin binding were due to a significant reduction in the maximum specific binding capacity with no change in the apparent binding constant. The data presented here are consistent with the hypothesis that MAO inhibitors reduce [3H]-serotonin binding indirectly, by increasing over time the exposure of serotonin receptors to the indolealkylamine.