Department of Comparative Medicine and Graduate Program in Molecular and Cellular Biology, University of Washington, Seattle, Washington 98195, USA.
Synapse. 2012 Dec;66(12):1024-34. doi: 10.1002/syn.21608. Epub 2012 Sep 29.
Serotonin-1B (5-HT(1B) ) autoreceptors are located in serotonin (5-HT) terminals, along with serotonin transporters (SERT), and play a critical role in autoregulation of serotonergic neurotransmission and are implicated in disorders of serotonergic function, particularly emotional regulation. SERT modulates serotonergic neurotransmission by high-affinity reuptake of 5-HT. Alterations in SERT activity are associated with increased risk for depression and anxiety. Several neurotransmitter receptors are known to regulate SERT K(m) and V(max) , and previous work suggests that 5-HT(1B) autoreceptors may regulate 5-HT reuptake, in addition to modulating 5-HT release and synthesis. We used rotating disk electrode voltammetry to investigate 5-HT(1B) autoreceptor regulation of SERT-mediated 5-HT uptake into synaptosomes. The selective 5-HT(1B) antagonist SB224289 decreased SERT activity in synaptosomes prepared from wild-type but not 5-HT(1B) knockout mice, whereas SERT uptake was enhanced after pretreatment with the selective 5-HT(1B) agonist CP94253. Furthermore, SERT activity varies as a function of 5-HT(1B) receptor expression-specifically, genetic deletion of 5-HT(1B) decreased SERT function, while viral-mediated overexpression of 5-HT(1B) autoreceptors in rat raphe neurons increased SERT activity in rat hippocampal synaptosomes. Considered collectively, these results provide evidence that 5-HT(1B) autoreceptors regulate SERT activity. Because SERT clearance rate varies as a function of 5-HT(1B) autoreceptor expression levels and is modulated by both activation and inhibition of 5-HT(1B) autoreceptors, this dynamic interaction may be an important mechanism of serotonin autoregulation with therapeutic implications.
5-羟色胺 1B(5-HT(1B))自身受体位于 5-羟色胺(5-HT)末梢中的 5-HT 转运体(SERT)附近,在 5-羟色胺能神经传递的自身调节中起着关键作用,并且与 5-羟色胺能功能障碍有关,特别是情绪调节。SERT 通过高亲和力摄取 5-HT 来调节 5-羟色胺能神经传递。SERT 活性的改变与抑郁和焦虑的风险增加有关。已知几种神经递质受体可调节 SERT K(m)和 V(max),先前的工作表明,5-HT(1B)自身受体除了调节 5-HT 释放和合成外,还可能调节 5-HT 再摄取。我们使用旋转圆盘电极伏安法研究了 5-HT(1B)自身受体对突触小体中 SERT 介导的 5-HT 摄取的调节作用。选择性 5-HT(1B)拮抗剂 SB224289 降低了来自野生型但不来自 5-HT(1B)敲除小鼠的突触小体中的 SERT 活性,而在预先用选择性 5-HT(1B)激动剂 CP94253 处理后,SERT 摄取增强。此外,SERT 活性随 5-HT(1B)受体表达而变化——具体而言,5-HT(1B)的基因缺失降低了 SERT 功能,而在大鼠中脑缝核神经元中病毒介导的 5-HT(1B)自身受体过表达增加了大鼠海马突触小体中的 SERT 活性。综合这些结果,提供了 5-HT(1B)自身受体调节 SERT 活性的证据。由于 SERT 清除率随 5-HT(1B)自身受体表达水平的变化而变化,并且受到 5-HT(1B)自身受体的激活和抑制的调节,这种动态相互作用可能是 5-羟色胺自身调节的一个重要机制,具有治疗意义。