Cortisol modulation of 5-HT-mediated growth hormone release in recovered depressed patients

被引:13
作者
Bhagwagar, Z [1 ]
Hafizi, S [1 ]
Cowen, PJ [1 ]
机构
[1] Univ Oxford, Warneford Hosp, Dept Psychiat, Oxford OX3 7JX, England
关键词
depression; cortisol; serotonin; growth hormone; tryptophan;
D O I
10.1016/S0165-0327(01)00467-0
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Background: Recent formulations of the pathophysiology of major depression suggest that stress-induced cortisol secretion may lower brain serotonin (5-HT) function, thereby precipitating depressive symptomatology. This implies that people who develop depression after stressful life events may be particularly vulnerable to the effect of cortisol on brain 5-HT activity. We therefore assessed the effect of a single dose of hydrocortisone on 5-HT-mediated growth hormone (GH) release in healthy volunteers and euthymic subjects recovered from at least two episodes of major depression. Methods: Eleven recovered depressed patients and 20 healthy controls received intravenous tryptophan (TRP) 10.5 h after placebo and hydrocortisone (50 ring orally) in a double-blind, cross-over design. Plasma GH levels were sampled for 90 min after TRP infusion. Results: The GH response to TRP was significantly lower in the recovered depressed patients than controls after hydrocortisone. Limitations: The number of recovered depressed subjects studied was small and the effect of hydrocortisone on TRP-induced GH release was different to that observed in a previous study. Conclusions: These findings are consistent with other evidence suggesting abnormal regulation of 5-HT neurotransmission in people vulnerable to recurrent depression. (C) 2002 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:249 / 255
页数:7
相关论文
共 17 条
[2]   Back to the future: The neurobiology of major depression [J].
Cowen, PJ .
PSYCHOLOGICAL MEDICINE, 1998, 28 (02) :253-255
[3]  
DEAKIN J F W, 1991, Journal of Psychopharmacology, V5, P305, DOI 10.1177/026988119100500414
[4]   A NEUROENDOCRINE STUDY OF 5HT FUNCTION IN DEPRESSION - EVIDENCE FOR BIOLOGICAL MECHANISMS OF ENDOGENOUS AND PSYCHOSOCIAL CAUSATION [J].
DEAKIN, JFW ;
PENNELL, I ;
UPADHYAYA, AJ ;
LOFTHOUSE, R .
PSYCHOPHARMACOLOGY, 1990, 101 (01) :85-92
[5]   GLUCOCORTICOIDS AND THE GENESIS OF DEPRESSIVE-ILLNESS - A PSYCHOBIOLOGICAL MODEL [J].
DINAN, TG .
BRITISH JOURNAL OF PSYCHIATRY, 1994, 164 :365-371
[6]   CONCEPTUALIZATION AND RATIONALE FOR CONSENSUS DEFINITIONS OF TERMS IN MAJOR DEPRESSIVE DISORDER - REMISSION, RECOVERY, RELAPSE, AND RECURRENCE [J].
FRANK, E ;
PRIEN, RF ;
JARRETT, RB ;
KELLER, MB ;
KUPFER, DJ ;
LAVORI, PW ;
RUSH, AJ ;
WEISSMAN, MM .
ARCHIVES OF GENERAL PSYCHIATRY, 1991, 48 (09) :851-855
[7]   The corticosteroid receptor hypothesis of depression [J].
Holsboer, F .
NEUROPSYCHOPHARMACOLOGY, 2000, 23 (05) :477-501
[8]   Blockade of corticosterone synthesis reduces serotonin turnover in the dorsal hippocampus of the rat as measured by microdialysis [J].
KorteBouws, GAH ;
Korte, SM ;
DeKloet, ER ;
Bohus, B .
JOURNAL OF NEUROENDOCRINOLOGY, 1996, 8 (11) :877-881
[9]  
MELTZER HY, 1988, CURRENT TOPICS NEURO, P183
[10]   TREATMENT OF MAJOR-DEPRESSION WITH METYRAPONE AND HYDROCORTISONE [J].
ODWYER, AM ;
LIGHTMAN, SL ;
MARKS, MN ;
CHECKLEY, SA .
JOURNAL OF AFFECTIVE DISORDERS, 1995, 33 (02) :123-128