Eser Daniela, di Michele Flavia, Zwanzger Peter, Pasini Augusto, Baghai Thomas C, Schüle Cornelius, Rupprecht Rainer, Romeo Elena
Department of Psychiatry, Ludwig-Maximilian-University, Munich, Germany.
Neuropsychopharmacology. 2005 Jan;30(1):192-5. doi: 10.1038/sj.npp.1300572.
3alpha-reduced neuroactive steroids such as 3alpha, 5alpha-tetrahydroprogesterone (3alpha, 5alpha-THP) and 3alpha, 5alpha-tetrahydrodeoxycorticosterone (3alpha, 5alpha-THDOC) are potent positive allosteric modulators of gamma-aminobutyric acid type A (GABAA) receptors and display pronounced anxiolytic activity in animal models. Experimental panic induction with cholecystokinin-tetrapeptide (CCK-4) and sodium lactate is accompanied by a decrease in 3alpha, 5alpha-THP concentrations in patients with panic disorder, but not in healthy controls. However, no data are available on 3alpha, 5alpha-THDOC concentrations during experimental panic induction. Therefore, we quantified 3alpha, 5alpha-THDOC concentrations in 10 healthy volunteers (nine men, one woman) before and after panic induction with CCK-4 by means of a highly sensitive and specific gas chromatography/mass spectrometry analysis. CCK-4 elicited a strong panic response as assessed by the Acute Panic Inventory. This was accompanied by an increase in 3alpha, 5alpha-THDOC, ACTH and cortisol concentrations. This increase in 3alpha, 5alpha-THDOC might be a consequence of hypothalamic-pituitary-adrenal (HPA) axis activation following CCK-4-induced panic, and might contribute to the termination of the anxiety/stress response following challenge with CCK-4 through enhancement of GABAA receptor function.
3α-还原神经活性甾体,如3α,5α-四氢孕酮(3α,5α-THP)和3α,5α-四氢脱氧皮质酮(3α,5α-THDOC),是γ-氨基丁酸A型(GABAA)受体的强效正性变构调节剂,在动物模型中表现出明显的抗焦虑活性。用胆囊收缩素四肽(CCK-4)和乳酸钠进行实验性惊恐诱导时,惊恐障碍患者的3α,5α-THP浓度会降低,但健康对照者不会。然而,关于实验性惊恐诱导期间3α,5α-THDOC浓度的数据尚无。因此,我们通过高灵敏度和特异性的气相色谱/质谱分析,对10名健康志愿者(9名男性,1名女性)在CCK-4诱导惊恐前后的3α,5α-THDOC浓度进行了定量。根据急性惊恐量表评估,CCK-4引发了强烈的惊恐反应。这伴随着3α,5α-THDOC、促肾上腺皮质激素(ACTH)和皮质醇浓度的升高。3α,5α-THDOC的这种升高可能是CCK-4诱导惊恐后下丘脑-垂体-肾上腺(HPA)轴激活的结果,并且可能通过增强GABAA受体功能,在CCK-4激发后促进焦虑/应激反应的终止。