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首页> 外文期刊>Human psychopharmacology: clinical and experimental >Decrease of the platelet 5-HT2A receptor function by long-term imipramine treatment in endogenous depression.
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Decrease of the platelet 5-HT2A receptor function by long-term imipramine treatment in endogenous depression.

机译：减少血小板5-HT2A受体的功能通过长期在内源性丙咪嗪治疗抑郁症。

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摘要

BACKGROUND: Animal studies have found that many antidepressants induce decreases in both the density and the functional activity of the serotonin 2A (5-HT(2A)) receptor subtype. However, the extrapolation of findings to humans has been inconclusive. A physiological platelet response mediated by this receptor, the serotonin-amplified platelet aggregation, was measured to study whether long-term antidepressant treatment induces changes in 5-HT(2A) receptor functioning in endogenous depressed patients. METHOD: The percentage of serotonin-amplified platelet aggregation to adenosine diphosphate (ADP) was studied in 15 untreated patients with major depressive disorder (DSM-IV) with endogenous features (Newcastle scale). This index was used as an indirect measurement of the functional status of platelet 5-HT(2A) receptors. Aggregation studies were repeated once remission of the symptoms was achieved during treatment with imipramine (150-300 mg/day). A group of 15 concurrent normal subjects was used as a control. RESULTS: A statistically significant decrease (p = 0.038) in the percentage of serotonin-amplified platelet aggregation to ADP was observed when remission was achieved (after 145 +/- 27 days). CONCLUSIONS: The results showed a decrease in a platelet functional response mediated by 5-HT(2A) receptors following effective imipramine treatment, suggesting that desensitization or down-regulation of the 5-HT(2A) receptor function could be linked to the therapeutic effect of some antidepressants. The data also support the use of platelet aggregometry as a surrogate measurement of antidepressant action, particularly in intra-subject designs.
机译：背景:动物研究发现,许多抗抑郁药物诱导的减少密度的机能活动5 -羟色胺2 a (5 - (2 a)受体亚型。然而,人类发现的外推一直不确定。响应由这种受体serotonin-amplified血小板聚集,衡量是否长期学习抗抑郁药物治疗引起的变化在内源性5 - (2 a)受体功能抑郁症患者。serotonin-amplified血小板聚集,二磷酸腺苷(ADP)研究了15个未经治疗的重度抑郁症患者(dsm - iv)与内生特性(纽卡斯尔规模)。测定的血小板的功能状态5 - (2 a)受体。重复一次缓解症状实现与丙咪嗪治疗期间(150 - 300毫克/天)。受试者被用作控制。显著减少(p = 0.038)serotonin-amplified血小板的百分比聚合时观察ADP缓解实现(145 + / - 27天后)。结论:结果显示下降血小板功能响应由5 - (2)受体后有效丙咪嗪治疗,表明脱敏的下调5 - (2 a)受体的功能的治疗效果可能与一些吗抗抑郁药。血小板aggregometry作为替代测量抗抑郁作用,特别是在intra-subject设计。

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