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The regulation of hypothalamic corticotropin releasing

  • Department of Neurobiology and Biophysics, School of Life Science, University of Science and Technology of China, Hefei 230027, China

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  • Corresponding author: ZHOU Jiang-ning, E-mail: jnzhou@ustc.edu.cn
  • Received Date: 28 June 2008
  • Rev Recd Date: 08 July 2008
  • Publish Date: 31 August 2008
    Abstract

  • Abstract

    Our recent studies reported that the expression of estrogen receptor (ER) and androgen receptor (AR) in corticotropin-releasing hormone (CRH) neurons in the paraventricular nucleus (PVN) of hypothalamus increases in depressed patients. Estrogen and androgen can modulate the transcription activity of CRH by binding ER or AR, which act on the estrogen response elements (EREs) and androgen response elements (AREs) on the human CRH gene promoter respectively. Androgen inhibits the activity of the CRH gene promoter while estrogen activates CRH gene expression. In addition to ER and AR, multiple receptors in the hypothalamus which regulate the activity of CRH neurons show a disturbed balance in depressed patients. Drug targeting to glucocorticoid receptors and sex hormone receptors might be useful for improving depressive behavior by modulating the neurons of different areas in the hippocampus. Based on these findings, we proposed the hypothesis that imbalances of multiple receptors in the hypothalamus may contribute to depression.

    Abstract

    Our recent studies reported that the expression of estrogen receptor (ER) and androgen receptor (AR) in corticotropin-releasing hormone (CRH) neurons in the paraventricular nucleus (PVN) of hypothalamus increases in depressed patients. Estrogen and androgen can modulate the transcription activity of CRH by binding ER or AR, which act on the estrogen response elements (EREs) and androgen response elements (AREs) on the human CRH gene promoter respectively. Androgen inhibits the activity of the CRH gene promoter while estrogen activates CRH gene expression. In addition to ER and AR, multiple receptors in the hypothalamus which regulate the activity of CRH neurons show a disturbed balance in depressed patients. Drug targeting to glucocorticoid receptors and sex hormone receptors might be useful for improving depressive behavior by modulating the neurons of different areas in the hippocampus. Based on these findings, we proposed the hypothesis that imbalances of multiple receptors in the hypothalamus may contribute to depression.
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    • References(79)
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    [1]
    王金荣, 王德平. 中国七个地区情感性精神障碍流行病学调查[J]. 中华精神科杂志, 1998, 31(2):75-77.
    [2]
    陆林, 黄明生. 三所精神病院住院患者的抑郁性障碍患病率的调查[J]. 中华精神科杂志, 1999, 32(4):236-238.
    [3]
    Chen R, Hu Z, Qin X, et al. A community-based study of depression in older people in Hefei, China: The GMS-AGECAT prevalence, case validation and socio-economic correlates[J]. Int J Geriatr Psychiatry, 2004, 19(5):407-413.
    [4]
    Liu C Y, Wang S J, Teng E L, et al. Depressive disorders among older residents in a Chinese rural community[J]. Psychol Med, 1997, 27(4):943-949.
    [5]
    Lee D, Yip A, Chiu H, et al. A psychiatric epidemiological study of postpartum Chinese women[J]. Am J Psychiatry, 2001, 158(2):220-226.
    [6]
    Keller M B. Past, present, and future directions for defining optimal treatment outcome in depression: remission and beyond[J]. Jama, 2003, 289(23):3 152-3 160.
    [7]
    Holden C. Future brightening for depression treatments[J]. Science, 2003, 302(5646):810-813.
    [8]
    Holsboer F. The corticosteroid receptor hypothesis of depression[J]. Neuropsychopharmacology, 2000, 23(5):477-501.
    [9]
    Stenzel-Poore M P, Heinrichs S C, Rivest S, et al. Overproduction of corticotropin-releasing factor in transgenic mice: a genetic model of anxiogenic behavior[J]. J Neurosci, 1994, 14(5 Pt 1):2 579-2 584.
    [10]
    Flores B H, Kenna H, Keller J, et al. Clinical and biological effects of mifepristone treatment for psychotic depression[J]. Neuropsychopharmacology, 2006, 31(3):628-636.
    [11]
    Young E A, Lopez J F, Murphy-Weinberg V, et al. Mineralocorticoid receptor function in major depression[J]. Arch Gen Psychiatry, 2003, 60(1):24-28.
    [12]
    Reus V I, Wolkowitz O M, Frederick S. Antiglucocorticoid treatments in psychiatry[J]. Psychoneuroendocrinology, 1997, 22 Suppl 1:S121-124.
    [13]
    Bao A M, Meynen G, Swaab D F. The stress system in depression and neurodegeneration: Focus on the human hypothalamus[J]. Brain Res Rev, 2008,57(2):531-553.
    [14]
    Wu L M, Han H, Wang Q N, et al. Mifepristone repairs region-dependent alteration of synapsin I in hippocampus in rat model of depression[J]. Neuropsychopharmacology, 2007, 32(12):2 500-2 510.
    [15]
    Huttner W B, Schiebler W, Greengard P, et al. Synapsin I (protein I), a nerve terminal-specific phosphoprotein. III. Its association with synaptic vesicles studied in a highly purified synaptic vesicle preparation[J]. J Cell Biol, 1983, 96(5):1 374-1 388.
    [16]
    De Camilli P, Benfenati F, Valtorta F, et al. The synapsins[J]. Annu Rev Cell Biol, 1990, 6:433-460.
    [17]
    Thiel G. Synapsin I, synapsin II, and synaptophysin: marker proteins of synaptic vesicles[J]. Brain Pathol, 1993, 3(1):87-95.
    [18]
    Pawlak R, Rao B S, Melchor J P, et al. Tissue plasminogen activator and plasminogen mediate stress-induced decline of neuronal and cognitive functions in the mouse hippocampus[J]. Proc Natl Acad Sci U S A, 2005, 102(50):18 201-18 206.
    [19]
    Cadepond F, Ulmann A, Baulieu E E. RU486 (mifepristone): Mechanisms of action and clinical uses[J]. Annu Rev Med, 1997, 48:129-156.
    [20]
    Magarinos A M, McEwen B S, Flugge G, et al. Chronic psychosocial stress causes apical dendritic atrophy of hippocampal CA3 pyramidal neurons in subordinate tree shrews[J]. J Neurosci, 1996, 16(10):3 534-3 540.
    [21]
    Krugers H J, Goltstein P M, van der Linden S, et al. Blockade of glucocorticoid receptors rapidly restores hippocampal CA1 synaptic plasticity after exposure to chronic stress[J]. Eur J Neurosci, 2006, 23(11):3 051-3 055.
    [22]
    Sheng Z, Yanai A, Fujinaga R, et al. Gonadal and adrenal effects on the glucocorticoid receptor in the rat hippocampus, with special reference to regulation by estrogen from an immunohistochemical view-point[J]. Neurosci Res, 2003, 46(2):205-218.
    [23]
    Sun H, Cheng X P, You-Ye Z, et al. Quercetin subunit specifically reduces GlyR-mediated current in rat hippocampal neurons[J]. Neuroscience, 2007, 148(2):548-559.
    [24]
    Bao A M, Ji Y F, van Someren E J, et al. Diurnal rhythms of free estradiol and cortisol during the normal menstrual cycle in women with major depression[J]. Horm Behav, 2004, 45(2):93-102.
    [25]
    Bao A M, Liu R Y, van Someren E J, et al. Diurnal rhythm of free estradiol during the menstrual cycle[J]. Eur J Endocrinol, 2003, 148(2):227-232.
    [26]
    Lund T D, Munson D J, Haldy M E, et al. Androgen inhibits, while oestrogen enhances, restraint-induced activation of neuropeptide neurones in the paraventricular nucleus of the hypothalamus[J]. J Neuroendocrinol, 2004, 16(3):272-278.
    [27]
    Seale J V, Wood S A, Atkinson H C, et al. Gonadectomy reverses the sexually diergic patterns of circadian and stress-induced hypothalamic-pituitary-adrenal axis activity in male and female rats[J]. J Neuroendocrinol, 2004, 16(6):516-524.
    [28]
    Bao A M, Hestiantoro A, Van Someren E J, et al. Colocalization of corticotropin-releasing hormone and oestrogen receptor-alpha in the paraventricular nucleus of the hypothalamus in mood disorders[J]. Brain, 2005, 128(Pt 6):1 301-1 313.
    [29]
    Isgor C, Cecchi M, Kabbaj M, et al. Estrogen receptor beta in the paraventricular nucleus of hypothalamus regulates the neuroendocrine response to stress and is regulated by corticosterone[J]. Neuroscience, 2003, 121(4):837-845.
    [30]
    Hu X Y, Qin S, Lu Y P, et al. Decreased estrogen receptor-alpha expression in hippocampal neurons in relation to hyperphosphorylated tau in Alzheimer patients[J]. Acta Neuropathol, 2003, 106(3):213-220.
    [31]
    Lu Y P, Zeng M, Swaab D F, et al. Colocalization and alteration of estrogen receptor-alpha and -beta in the hippocampus in Alzheimers disease[J]. Hum Pathol, 2004, 35(3):275-280.
    [32]
    Gustafsson J A. What pharmacologists can learn from recent advances in estrogen signalling[J]. Trends Pharmacol Sci, 2003, 24(9):479-485.
    [33]
    Vamvakopoulos N C, Chrousos G P. Evidence of direct estrogenic regulation of human corticotropin-releasing hormone gene expression. Potential implications for the sexual dimophism of the stress response and immune/inflammatory reaction[J]. J Clin Invest, 1993, 92(4):1 896-1 902.
    [34]
    Dibbs K I, Anteby E, Mallon M A, et al. Transcriptional regulation of human placental corticotropin-releasing factor by prostaglandins and estradiol[J]. Biol Reprod, 1997, 57(6):1 285-1 292.
    [35]
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