酒精中毒[纠正：alcolholism应改为alcoholism]中皮质醇与血清素代谢物及转运体之间的关系
Relationship between cortisol and serotonin metabolites and transporters in alcoholism [correction of alcolholism].
作者信息
Heinz A, Jones D W, Bissette G, Hommer D, Ragan P, Knable M, Wellek S, Linnoila M, Weinberger D R
机构信息
Intramural Research Program, Clinical Brain Disorders Branch/NIMH, Bethesda, MD, USA.
出版信息
Pharmacopsychiatry. 2002 Jul;35(4):127-34. doi: 10.1055/s-2002-33197.
BACKGROUND
Stress hormone activation may induce clinical depression via an interference with central serotonergic neurotransmission. In alcoholics, a reduction in serotonin transporters was associated with clinical depression, and an activation of cortisol secretion is frequently found during detoxification. We assessed the interaction between stress hormone activation, serotonin transporters, monoamine metabolites in the cerebrospinal fluid (CSF), and mood states in male and female alcoholics and healthy control subjects.
METHODS
The availability of serotonin transporters was measured with [I-123]beta-CIT and SPECT in the raphe area of the brainstem in 31 alcoholics after four weeks of abstinence and in 25 age-matched healthy volunteers. Concentrations of plasma cortisol were measured on the day of the SPECT scan. Within one week after the SPECT scan, we assessed monoamine metabolites and corticotropin-releasing factor (CRF) in the CSF.
RESULTS
Clinical depression was associated with a reduction in serotonin transporter availability among male alcoholics. Among male alcoholics and healthy volunteers, CSF 5-HIAA and plasma cortisol concentrations were inversely correlated with the availability of raphe serotonin transporters and positively correlated with the severity of clinical depression. No significant correlations were observed between raphe serotonin transporters and HVA, MHPG and CRF concentrations in the CSF.
CONCLUSION
Our findings support the hypothesis of an interaction between reduced serotonin transporters, stress hormone activation and clinical depression. They confirm the hypothesis that serotonergic neurotransmission dysfunction in alcoholism is limited to male alcoholics. The observed interactions between high cortisol concentrations and reduced serotonin transporter availability warrant further studies in major depression and other neuropsychiatric diseases with implied cortisol activation and serotonergic dysfunction.
背景
应激激素激活可能通过干扰中枢5-羟色胺能神经传递而诱发临床抑郁症。在酗酒者中，5-羟色胺转运体减少与临床抑郁症相关，且在戒酒期间经常发现皮质醇分泌激活。我们评估了应激激素激活、5-羟色胺转运体、脑脊液（CSF）中的单胺代谢产物以及男性和女性酗酒者与健康对照者情绪状态之间的相互作用。
方法
用[I-123]β-CIT和单光子发射计算机断层扫描（SPECT）测量了31名戒酒四周的酗酒者和25名年龄匹配的健康志愿者脑干中缝核区域5-羟色胺转运体的可用性。在SPECT扫描当天测量血浆皮质醇浓度。在SPECT扫描后一周内，我们评估了CSF中的单胺代谢产物和促肾上腺皮质激素释放因子（CRF）。
结果
临床抑郁症与男性酗酒者5-羟色胺转运体可用性降低相关。在男性酗酒者和健康志愿者中，CSF中5-羟吲哚乙酸（5-HIAA）和血浆皮质醇浓度与中缝核5-羟色胺转运体的可用性呈负相关，与临床抑郁症的严重程度呈正相关。未观察到中缝核5-羟色胺转运体与CSF中高香草酸（HVA）、3-甲氧基-4-羟基苯乙二醇（MHPG）和CRF浓度之间存在显著相关性。
结论
我们的研究结果支持5-羟色胺转运体减少、应激激素激活与临床抑郁症之间相互作用的假说。它们证实了酗酒中5-羟色胺能神经传递功能障碍仅限于男性酗酒者的假说。观察到的高皮质醇浓度与5-羟色胺转运体可用性降低之间的相互作用值得在重度抑郁症和其他伴有皮质醇激活和5-羟色胺能功能障碍的神经精神疾病中进行进一步研究。
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