Pinna Graziano
Department of Psychiatry, College of Medicine, The Psychiatric Institute, University of Illinois at Chicago, Chicago, Illinois 60612, USA.
Behav Pharmacol. 2010 Sep;21(5-6):438-50. doi: 10.1097/FBP.0b013e32833d8ba0.
The pathophysiological role of the neurosteroid 3alpha-hydroxy-5alpha-pregnan-20-one (allopregnanolone) in neuropsychiatric disorders has been highlighted in several recent investigations. For instance, allopregnanolone levels are decreased in the CSF of patients with post-traumatic stress disorder (PTSD) and major unipolar depression. Neurosteroidogenic antidepressants, including fluoxetine and analogs, correct this decrease in a manner that correlates with improved depressive symptoms. PTSD-like behavioral dysfunctions, including heightened aggression, exaggerated fear, and anxiety-like behavior associated with a decrease in corticolimbic allopregnanolone content are modeled in mice by protracted social isolation stress. Allopregnanolone is not only synthesized by principal glutamatergic and gamma-aminobutyric acid (GABA)ergic neurons, but also locally, potently, positively, and allosterically modulates GABA action at postsynaptic and extrasynaptic GABAA receptors. Hence, this paper will review preclinical studies, which show that in socially isolated mice, rather than selective serotonin reuptake inhibitor mechanisms, allopregnanolone biosynthesis in glutamatergic corticolimbic neurons offers a nontraditional target for fluoxetine to decrease signs of aggression, normalize fear responses, and decrease anxiety-like behavior. At low selective serotonin reuptake inhibitor-inactive doses, fluoxetine and related congeners potently increase allopregnanolone levels by acting as potent selective brain steroidogenic stimulants (SBSS), thereby facilitating GABAA receptor neurotransmission and improving behavioral dysfunctions. Although the precise molecular mechanisms that underlie the action of these drugs are not fully understood, findings from socially isolated mice may ultimately generate insights into novel drug targets for the treatment of psychiatric disorders, such as anxiety and panic disorders, depression, and PTSD.
神经甾体3α-羟基-5α-孕烷-20-酮(别孕烯醇酮)在神经精神疾病中的病理生理作用在最近的几项研究中得到了凸显。例如,创伤后应激障碍(PTSD)和重度单相抑郁症患者的脑脊液中别孕烯醇酮水平降低。包括氟西汀及其类似物在内的神经甾体生成性抗抑郁药以与改善抑郁症状相关的方式纠正了这种降低。通过长期社会隔离应激在小鼠中模拟了PTSD样行为功能障碍,包括攻击性增强、恐惧过度以及与皮质边缘别孕烯醇酮含量降低相关的焦虑样行为。别孕烯醇酮不仅由主要的谷氨酸能和γ-氨基丁酸(GABA)能神经元合成,而且还在局部对突触后和突触外GABAA受体处的GABA作用进行强效、正向和变构调节。因此,本文将综述临床前研究,这些研究表明,在社会隔离的小鼠中,谷氨酸能皮质边缘神经元中的别孕烯醇酮生物合成提供了一个非传统靶点,使氟西汀能够减少攻击迹象、使恐惧反应正常化并减少焦虑样行为,而不是通过选择性5-羟色胺再摄取抑制剂机制。在低剂量的无选择性5-羟色胺再摄取抑制活性的情况下,氟西汀及相关同系物通过作为强效选择性脑甾体生成刺激剂(SBSS)来有效提高别孕烯醇酮水平,从而促进GABAA受体神经传递并改善行为功能障碍。尽管这些药物作用的精确分子机制尚未完全了解,但社会隔离小鼠的研究结果最终可能为治疗精神疾病(如焦虑症和恐慌症、抑郁症和PTSD)的新药物靶点提供见解。