Roehr J, Woods A, Corbett R, Kongsamut S
Department of Biological Research, Hoechst-Roussel Pharmaceuticals Inc., Somerville, NJ 08876, USA.
Eur J Pharmacol. 1995 May 4;278(1):75-8. doi: 10.1016/0014-2999(95)00099-7.
Schedule-induced polydipsia was induced when food-deprived rats were subjected to a fixed-time (60 s) feeding schedule for 150 min daily for 3 weeks (training period). Subsequent chronic administration of the serotonin reuptake inhibitor fluoxetine reduces schedule-induced polydipsia over 2-4 weeks. We asked whether changes in the serotonin reuptake carrier occur following the development of schedule-induced polydipsia and its reduction by fluoxetine. Using [3H]paroxetine binding, we found a 40% increase in Kd and a 50% decrease in Bmax in polydipsic rats; both were reversed by fluoxetine. Food deprivation alone did not affect these parameters. These observations suggest that changes in the serotonin reuptake carrier correlate with the development and reversal of schedule-induced polydipsia.
当剥夺食物的大鼠每天接受150分钟固定时间(60秒)的喂食计划,持续3周(训练期)时,会诱发日程诱导性烦渴。随后,连续2至4周长期给予血清素再摄取抑制剂氟西汀可减少日程诱导性烦渴。我们研究了日程诱导性烦渴形成及其被氟西汀减轻后,血清素再摄取载体是否发生变化。通过[3H]帕罗西汀结合实验,我们发现烦渴大鼠的解离常数(Kd)增加了40%,最大结合容量(Bmax)降低了50%;两者均被氟西汀逆转。单独的食物剥夺并不影响这些参数。这些观察结果表明,血清素再摄取载体的变化与日程诱导性烦渴的形成和逆转相关。