CNS Studies, Clinical Trials of Texas Research Center, San Antonio, TX, USA.
J Sex Med. 2017 Dec;14(12):1575-1584. doi: 10.1016/j.jsxm.2017.10.068.
The neurobiology of sexual response is driven in part by dopamine and serotonin-the former modulating excitatory pathways and the latter regulating inhibitory pathways. Neurobiological underpinnings of hypoactive sexual desire disorder (HSDD) are seemingly related to overactive serotonin activity that results in underactive dopamine activity. As such, pharmacologic agents that decrease serotonin, increase dopamine, or some combination thereof, have therapeutic potential for HSDD.
To review the role of serotonin in female sexual function and the effects of pharmacologic interventions that target the serotonin system in the treatment of HSDD.
Searches of the Medline database for articles on serotonin and female sexual function.
Relevant articles from the peer-reviewed literature were included.
Female sexual response is regulated not only by the sex hormones but also by several neurotransmitters. It is postulated that dopamine, norepinephrine, oxytocin, and melanocortins serve as key neuromodulators for the excitatory pathways, whereas serotonin, opioids, and endocannabinoids serve as key neuromodulators for the inhibitory pathways. Serotonin appears to be a key inhibitory modulator of sexual desire, because it decreases the ability of excitatory systems to be activated by sexual cues. Centrally acting drugs that modulate the excitatory and inhibitory pathways involved in sexual desire (eg, bremelanotide, bupropion, buspirone, flibanserin) have been investigated as treatment options for HSDD. However, only flibanserin, a multifunctional serotonin agonist and antagonist (5-hydroxytryptamine [5-HT] receptor agonist and 5-HT receptor antagonist), is currently approved for the treatment of HSDD.
The central serotonin system is 1 biochemical target for medications intended to treat HSDD.
This narrative review integrates findings from preclinical studies and clinical trials to elucidate neurobiological underpinnings of HSDD but is limited to 1 neurotransmitter system (serotonin).
Serotonin overactivity is a putative cause of sexual dysfunction in patients with HSDD. The unique pharmacologic profile of flibanserin tones down inhibitory serotonergic function and restores dopaminergic and noradrenergic function. Croft HA. Understanding the Role of Serotonin in Female Hypoactive Sexual Desire Disorder and Treatment Options. J Sex Med 2017;14:1575-1584.
性反应的神经生物学部分受多巴胺和 5-羟色胺驱动——前者调节兴奋性通路，后者调节抑制性通路。低性欲性障碍（HSDD）的神经生物学基础似乎与活性过强的 5-羟色胺活性有关，这种活性导致多巴胺活性降低。因此，减少 5-羟色胺、增加多巴胺或两者结合的药物在治疗 HSDD 方面具有治疗潜力。
综述 5-羟色胺在女性性功能中的作用，以及靶向 5-羟色胺系统的药物干预对 HSDD 的治疗作用。
在 Medline 数据库中搜索关于 5-羟色胺和女性性功能的文章。
纳入了来自同行评议文献的相关文章。
女性性反应不仅受性激素调节，还受几种神经递质调节。据推测，多巴胺、去甲肾上腺素、催产素和黑色素皮质素作为兴奋性通路的关键神经调节剂，而 5-羟色胺、阿片类药物和内源性大麻素作为抑制性通路的关键神经调节剂。5-羟色胺似乎是性欲的关键抑制性调节剂，因为它降低了兴奋性系统对性线索的激活能力。已经研究了调节性欲涉及的兴奋性和抑制性通路的中枢作用药物（例如，布雷美尔肽、安非他酮、丁螺环酮、氟班色林）作为 HSDD 的治疗选择。然而，只有氟班色林，一种多功能 5-羟色胺激动剂和拮抗剂（5-羟色胺[5-HT]受体激动剂和 5-HT 受体拮抗剂），目前被批准用于治疗 HSDD。
中枢 5-羟色胺系统是治疗 HSDD 药物的 1 个生化靶点。
本叙事综述整合了临床前研究和临床试验的结果，阐明了 HSDD 的神经生物学基础，但仅限于 1 个神经递质系统（5-羟色胺）。
5-羟色胺活性过强是 HSDD 患者性功能障碍的一个潜在原因。氟班色林独特的药理学特征抑制了抑制性 5-羟色胺能功能，恢复了多巴胺能和去甲肾上腺素能功能。
