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首页> 外文期刊>Life sciences >Enhancement in extracellular serotonin levels by 5-hydroxytryptophan loading after administration of WAY 100635 and fluoxetine.
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Enhancement in extracellular serotonin levels by 5-hydroxytryptophan loading after administration of WAY 100635 and fluoxetine.

机译：服用WAY 100635和氟西汀后，通过5-羟色氨酸负载增强细胞外血清素水平。

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摘要

It has been demonstrated that synthesis of serotonin (5-HT) is dependent on the availability of precursor, as well as the activity of 5-HT neurons. In the present series of experiments, we examined the effects of precursor (5-HTP) loading on extracellular hypothalamic 5-HT after administration of fluoxetine alone or in combination with WAY 100635, a selective 5-HT1A antagonist. In the first experiment, fluoxetine alone (10 mg/kg i.p.) caused 5-HT levels to significantly increase to 150% of basal levels. Subsequent administration of 5-HTP at 10, 20, and 40 mg/kg i.p. caused 5-HT levels to further increase to a maximum value of 254%, 405%, and 618%, respectively. In the second experiment, either vehicle or WAY 100635 (1 mg/kg/hour s.c.) was infused, then fluoxetine (10 mg/kg i.p.) and 5-HTP (10 mg/kg i.p.) were administered. By itself, WAY 100635 led to a slight but significant increase in hypothalamic 5-HT levels one hour after the start of administration (130% of basal levels). In the WAY 100635-treated group, fluoxetine caused an increase to 240% of basal levels after one hour, which rose to 290% of basal levels after two hours. Subsequent administration of 5-HTP further increased 5-HT levels to 580% of basal levels after one hour. In the vehicle-treated group, fluoxetine caused an increase of 160% of basal levels which was stable over two hours, and subsequent administration of 5-HTP led to a slight increase in 5-HT levels of 220% after one hour. These results suggest that combining blockade of 5-HT1A autoreceptors with 5-HT uptake inhibition results in a synergistic increase in synthesis and release of 5-HT when precursor is administered.
机译：已经证明5-羟色胺（5-HT）的合成取决于前体的可用性以及5-HT神经元的活性。在本系列实验中，我们检查了单独使用氟西汀或与选择性5-HT1A拮抗剂WAY 100635联合使用后，前体（5-HTP）负载对细胞外下丘脑5-HT的影响。在第一个实验中，仅氟西汀（10 mg / kg i.p.）导致5-HT水平显着增加至基础水平的150％。随后以10、20和40 mg / kg腹膜内注射5-HTP。导致5-HT水平进一步分别上升至最大值254％，405％和618％。在第二个实验中，注入媒介物或WAY 100635（1 mg / kg /小时s.c.），然后服用氟西汀（10 mg / kg i.p.）和5-HTP（10 mg / kg i.p.）。在给药开始后一小时，WAY 100635本身导致下丘脑5-HT水平轻微但显着增加（基础水平的130％）。在WAY 100635处理组中，氟西汀引起一小时后基础水平增加至240％，两小时后上升至基础水平的290％。一小时后，随后施用5-HTP将5-HT水平进一步提高至基础水平的580％。在赋形剂治疗组中，氟西汀引起基础水平增加160％，在两个小时内保持稳定，随后施用5-HTP导致一小时后5-HT水平轻微增加220％。这些结果表明，将5-HT1A自身受体的阻断与5-HT摄取抑制相结合，可以在施用前体时协同提高5-HT的合成和释放。

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