摘要
CRH、ACTH、NPY和GAL在抑郁症发病中作用
及其机制的研究
抑郁症（depression），又称单相情感性障碍（minor depression），是以显著而
持久的抑郁情感或心境改变为主要特征的一组疾病，也是与应激密切相关的一类
精神病。部队指战员无论平时还是战时都处于不同程度的应激状态，其抑郁症的
发病率高于一般群体。抑郁症已严重威胁指战员身心健康，是造成部队非战斗减
员的重要因素之一。随着社会竞争的日益加剧，在日常生活、学习和工作中，人
们承受的生理、心理压力越来越大，抑郁症的发病率有不断升高的趋势。因此，
加强对应激尤其是军事应激所致抑郁症的研究，在平战时都具有十分重要的意义。
抑郁症发病机理的研究，虽然过去建立与发展了许多学说，但由于对抑郁症发
病机理没有彻底搞清，对抑郁症的诊断和治疗还存在许多问题。目前对抑郁症发
病机理的研究，以及筛选敏感而稳定的抑郁症早期诊断和疗效评价指标等，仍然
是研究的热点。
本研究应用行为测定、放射免疫分析、免疫组化、原位杂交等技术和方法，对
促肾上腺皮质激素释放激素（CRH）、促肾上腺皮质激素（ACTH）、甘丙肽（GAL）
和神经肽 Y（NPY）在抑郁症发病中的作用和机制，进行了较为系统的研究。首先
弄清抑郁症病人血浆中CRH、ACTH、GAL和NPY含量的变化。在此基础上，利用大
鼠抑郁症模型，研究这四种神经肽在抑郁症发病中的作用，并观察GAL和NPY受
体的效应分子GIRK在抑郁症时的变化。旨在观察抑郁症时神经肽CRH、ACTH、GAL
和NPY的变化规律，探讨平战时抑郁症早期诊断、疗效判断及预后评价的指标，
并进一步阐明神经肽参与抑郁症发病的可能机制，为临床抑郁症的诊断和防治提
供新的途径和实验依据。
本研究的主要结果和讨论：
一、抑郁症患者血浆CRH、ACTH、GAL和NPY含量的变化
一
与正常人群相比，中度和重度抑郁症患者血浆AC＊含量显著升高中＜0刀5入
重度抑郁症患者血浆＊PY含量显著降低中0刀1人所有抑郁症患者血浆0＊L含
量均显著升高巾功刀 1），并且有随着抑郁症状加重而升高的趋势。
二、大鼠抑郁症撞型的建立
利用长期电击足底应激，制备大鼠抑郁症模型。结果发现，本模型动物表现出
的抑郁状态、兴趣丧失、快感缺乏与抑郁症临床表现中的精神运动改变、兴趣或
快感的丧失有一定程度的相似性。实验表明，这是较为理想的抑郁症动物模型。
三、实验性抑郁症大鼠血桨和备脑区神经肚含量的变化
1．血浆和各脑区 CRH含量的变化 与对照组相比，抑郁症大鼠血浆CRH含
量无明显变化，下丘脑和垂体前叶CRH含量显著升高，海马、顶叶和额叶显著降
低。CRH神经元在脑内主要位于下丘脑。垂体前叶的CRH主要来源于下丘脑，提
示抑郁时垂体前叶CRH含量的升高很可能是下丘脑CRH合成增加的结果。抗抑
郁药盐酸氟西汀对血浆、海马、颖叶和顶叶的CRH水平无明显影响，但可显著降
低垂体前叶CRH的含量。表明抑郁症时，CRH含量在各脑区的变化不一致，抗抑
郁药对各脑区CRH含量的影响也有差异，提示CRH在不同的脑区可能有不同的
作用，其机制还有待于进一步研究。
2．血浆和各脑区ACTH含量的变化 与对照组相比，实验性抑郁症大鼠血浆
ACTH含量无明显变化，下丘脑AC＊含量显著下降，其次是海马和顶叶，而在
其它脑区未发现明显变化。与生理盐水组相比，盐酸氟西汀组大鼠海马的ACTH
含量有所上升，提示海马可能与盐酸氟西汀的抗抑郁作用有关。
3．血浆和各脑区 GAL含量的变化 与对照组相比，实验性抑郁症大鼠血浆GAL
的含量显著下降，与抑郁症患者血浆GAL含量显著升高正好相反，这可能是由于
人和鼠GAL的种属差异较大造成的。实验性抑郁症大鼠下丘脑、海马、额叶、顶
叶和前脑的GAL含量均显著下降，提示抑郁症时大鼠血浆GAL的含量下降，可能
是由于脑内这些区域GAL含量下降所致。给予抗抑郁治疗可显著升高抑郁症大鼠
海马和前脑GAL的含量，提示盐酸氟西汀可能通过影响这两个脑区GAL神经元而
改善抑郁症状，也表明海马和前脑在抑郁症发病中可能起着重要作用。
4．血浆和各脑区NPY fi的变化 与对照组相比，实验性抑郁症大鼠血浆的
NPY含量均显著降低，给予抗抑郁药治疗后，抑郁症大鼠血浆的NPY含量显著升高，
The Study on the Principle of CRH, ACTH, NPY and
GAL in Depression and its Mechanism
Depression is a series of disease characterized by remarkable and permanent
depressive mood or mental changes. The incidence of depression has increased
progressively for more and more social challenge these years. Depression has become a
major health concern not only because of personal distress, excess mortality, impaired
interpersonal relationships, and restriction of work activities but also because of the
economic burden it imposes. So it is very important to pay more attention to the study of
depression.
Although there were many hypothesis and theories, the mechanism of depression
remains confusing and has attracted considerable attention.
in this study we explored the role of neuropeptides CRH, ACTH, GAL and NPY in the
development of depression using R1A, immunohistochemistry, and in situ hybndyzation.
First, we examined the alteration of the contents of these neuropeptides in plasma of
depression patients. Then, we established a model of depression rats. Thereafter, we
investigated the alteration of the contents of these neuropeptides in plasma and different
brain regions of depression rats and studied the differences of expression of GIRK mRNAs,
the effector of these neuropeptides, in depression rats and in normal rats. This study would
clarify the mechanism of participation in depression of neuropeptides and contribute to early
diagnosis and judgement of prognosis of depression.
The main results are as follows:
1. The alteration of contents of neuropeptldes CRH, ACTH, GAL and NPY in
plasma of depression patients.
The contents of plasma ACTH markedly increased in moderate and heavy depression
patients (p of all the depression patients the contents of GAL obviously nsed and parrelleled with
degree of depression.
2. Establlshm nt of exp rim ntal d pressl n mod I
The d pr ssion model was established by chronic unpredictable mild stress. The animal
appeared depressiv b havioF, loss of int6rest and anhedonia, which were simiIar to the
diagnosis StandaFd of clinicaI depression. So it was an ideal depression modeI.
3.The changes of cont6nta of neuropeptldes in pIasma and dlff6rent brain
regions Of depression rata.
(1 ) CRH ln depression rats the cont6nts of CRH obviously increased in the
hypathalamus and anterior pitUitory a decreased in the hippocampus, parietaI Iobe and
t6mporal lobe of cerebraI cortex. CRH-positive neurons mainly diStribut6 in the
hypothalamus. So CRH in ant6rior pituitary came bom hypothaIamus. This suggest6d the
.
increase of CRH in ant6rior pituitary of depression ratS was the results of the increase of
CRH synthesis in hypothalamus. FIuox6tine hydroChIoride had no eff6Ct on the cont6nts Of
CRH in pIasma, hippacampus, pari6tal Iobe and t6mporal lobe Of cerebral cort6x, but
decreased the cont6ntS Of CRH in the ant6rior pituitery and increas6d that in the fOrebrain.
The dfferent changes of CRH in diff6rent brain regions in depression rats and different
etheCtS Of fluoxehne hydrachloride on the cont8ntS Of CRH in different brain regions indicat6d
CRH had diff6rent fUnCtions in different brain regions. The mechanism remains obscure.
(2) ACTH The cont6ntS Of ACTH of depression rats decreas6d more obviousIy in
hypothalamus than in the hippacampus and pariet8l Iobe of cerebraI cort6x, and f8iled to
aIt6r in other brain mpions. Aff6r adminiStration Of ffuox8tine hydrochloride the cont6nts of
ACTH in the hippacampus and pari6taI lobe of cerebraI cort6x of ratS increased. This
suggeSted hippaca
引文
1．程义勇，心理应激研究进展，医药卫生科学技术进展 军事医学科学出版社．1996；15：12-13
2．崔虹，军事飞行人员SCL-90评定结果分析 心理科学．1994；17：59
3. Kompier MAJ, Martino VD. Review of bus driver's occupational stress and stress prevention. Stress Med. 1995;11:253
4．甘景梨等，军校学员抑郁症状及有关因素调查。中国临床心理学杂志．1996；4：172
5．肖凉等，城市人群中抑郁症状及抑郁症的发病率调查分析。第三次中华医学会精神病学分会学术年会材料汇编．P168
6．沈渔村，精神病学，人民卫生出版社．1980 628
7．程义勇，心理应激研究进展，医药卫生科学技术进展 军事医学科学出版社．1996；15：14-15
8. Kompier MAJ, Martino VD. Review of bus driver's occupational stress and stress prevention. Stress Med. 1995;11:253
9. Jimenez Vasquez PA, Salmi P, Ahlenius S, Mathe AA. Neuropeptide Yin brains of the Flinders Sensitive Line rat, a model of depression.Effects of electroconvulsive stimuli and d-amphetamine on peptide concentrations and locomotion. Behav Brain Res 2000 Jun 15;111(1-2):115-23
10. Liu RY, Zhou JN, Hoogendijk WJ, van Heerikhuize J, Kamphorst W,Unmehopa UA, Hofman MA Swaab DF. Decreased vasopressin gene expression in the biological clock of Alzheimer disease patients with and without depression. J Neuropathol Exp Neurol 2000 Apr;59(4):314-22
11. Baby S, Nguyen M, Tran D, Raffa RB. Substance Pantagonists: the next breakthrough in treating depression? J Clin Pharm Ther 1999 Dec;24(6):461-9
12． Redei E, Organ M, Hart S. Antidepressant-like properties of prepro-TRH 178-199: acute effects in the forced swim test. Neuroreport 1999 Nov 8; 10(16) :3273-6
13． Zhang K, Hamanaka K, Kitayama I, Soya H, Yoshizato H, Nakase S, Uesugi Y, Inui K, Nomura J, Okazaki Y. Decreased expression of the mRNA for somatostatin in the periventricular nucleus of depression-model rats. Life Sci 1999;65(9) :PL87-94
14． Sundblom DM, Heikman P, Naukkarinen H, Fyhrquist F. Blood concentrations of vasopressin, neuropeptide FF and prolactin are increased by high-dose right unilateral ECT. Peptides 1999;20(3) :319-26
15． Castilla-Cortazar I, Castilla A, Gurpegui M. Opioid peptides and immunodysfunction in patients with major depression and anxiety disorders. J Physiol Biochem 1998 Dec;54(4) :203-15
16． Weiss JM, Bonsall RW, Demetrikopoulos MK, Emery MS, West CH. Galanin: a significant role in depression? Ann N Y Acad Sci 1998 Dec 21:863:364-82
17． Gold PW, Chrousos GP. The endocrinology of melancholic and atypical depression: relation to neurocircuitry and somatic consequences. Proc Assoc Am Physicians 1999 Jan-Feb; 111(1) :22-34
18． Arborelius L, Owens MJ, Plotsky PM, Nemeroff CB. The role of corticotropin-releasing factor in depression and anxiety disorders. J Endocrinol 1999 Jan;160(1) :1-12
19． Caberlotto L, Jimenez P, Overstreet DH, Hurd YL, Mathe AA, Fuxe K. Alterations in neuropeptide Y levels and Y1 binding sites in the Flinders Sensitive Line rats, a genetic animal model of depression. Neurosci Lett 1999 Apr 23;265(3) :191-4
20． Sattin A. A heuristic model of mental depression derived from basic and applied research on thyrotropin-releasing hormone. Thyroid 1998 Oct;8(10) :957-62
21． Dinan TG. Psychoneuroendocrinology of depression. Growth hormone Psychiatr Clin North Am 1998 Jun;21(2) :325-39
22． Hamanaka K, Soya H, Yoshizato H, Nakase S, Ono J, Inui K, Zhang K, Okuyama R, IshikawaY, Kitayama I, Nomura J. Enhanced response of growth hormone to growth hormone-releasing hormone and a decreased content of hypothalamic somatostatin in a stress-induced rat model of depression. J Neuroendocrinol 1998 Apr;10(4) :259-65
23． Warnock JK, Bundren JC, Morris DW. Sertraline in the treatment of depression associated with gonadotropin-releasing hormone agonist therapy. Biol Psychiatry 1998 Mar 15;43(6) :464-5
24． Krittayaphong R, Light KC, Golden RN, Finkel JB, Sheps DS. Relationship among depression scores, beta-endorphin, and angina pectoris during exercise in patients with coronary artery disease. Clin J Pain 1996 Jun;12(2) :126-33
25． Tejedor-Real P, Mico JA, Maldonado R, Roques BP, Gibert-Rahola J. Implication of endogenous opioid system in the learned helplessness model of depression. Pharmacol Biochem Behav 1995 Sep;52(1) :145-52
26． Amsterdam JD, Maislin G, Rosenzweig M, Halbrecht U. Gonadotropin (LH and FSH) response after submaximal GnRH stimulation in depressed premenopausal women and healthy controls. Psychoneuroendocrinology 1995;20(3) :311-21
27． Lieb K, Fiebich BL, Berger M. Substance P receptor antagonists梐 new antidepressive and anxiolytic mechanism Nervenarzt 2000 Sep;71(9) :758-61
28． Sven Ove Ogren , Par A. Schott, Jan Kehr, Ilga Misane, Haleh Razani Galanin and learning _ . Brain Research 848 1999 174-182
29． Gold PW, Chrousos GP. The endocrinology of melancholic and atypical depression: relation to neurocircuitry and somatic consequences. Proc Assoc Am Physicians 1999 Jan-Feb;111(1) :22-34
30． Sundblom DM, Heikman P, Naukkarinen H, Fyhrquist F. Blood concentrations of vasopressin, neuropeptide FF and prolactin are increased by high-dose right unilateral ECT. Peptides 1999;20(3) :319-26
31． Katz R. J. et al Acute and chronic stress effects on open field activity in the rat: implications for a model of depression. Neuroscience & biobehavioral Reviews 1981,5:247-251
32． Willner P, Benton D, Brown E, Cheeta S, Davies G, Morgan J, Morgan M: "Depression" increases "craving" for sweet rewards in animal and human models of depression and craving'. Psychopharmacology (Berl) 1998 ;136(3) :272-83
33． Willner P: Validity, reliability and utility of the chronic mild stress model of depression: a 10-year review and evaluation. Psychopharmacology (Berl) 1997 ;134 (4) :319-29
34． D'Aquila PS, Brain P, Willner P: Effects of chronic mild stress on performance in behavioural tests relevant to anxiety and depression. Physiol Behav 1994 ;56(5) :861-7
35． Rosenblum LA, Paully GS: Primate models of separation-induced depression. Psychiatr Clin North Am 1987;10(3) :437-47
36． Crawley JN: A monoamine oxidase inhibitor reverses the ' separation syndrome' in a new hamster separation model of depression. Eur J Pharmacol 1985:112(1) :129-33
37． Kamata K, Rebec GV: Nigral reticulata neurons: potentiation of responsiveness to amphetamine with long-term treatment. Brain Res 1985;332(1) :188-93
38． Kelly JP, Wrynn AS, Leonard BE: The olfactory bulbectomized rat as a model of depression: an update. Pharmacol Ther 1997;74(3) :299-316
39． Holmes PV, Davis RC, Masini CV, Primeaux SD: Effects of olfactory bulbectomy on neuropeptide gene expression in the rat olfactory/1imbic system. Neuroscience 1998 ;86(2) :587-96
40． Slotkin TA, Miller DB, Fumagalli F, McCook EC, Zhang J, Bissette G, eidler FJ: Modeling geriatric depression in animals: biochemical and behavioral effects of olfactory bulbectomy in young versus aged rats. J Pharmacol Exp Ther 1999 ;289(1) :334-45
41． Spiess J, Rivier J, Rivier C, Vale W. Primary structure of corticotropin-releasing factor from ovine hypothalamus Proc Natl Acad Sci USA 1981 Oct;78(10) :6517-21
42． Zhao L, Donaldson CJ, Smith GW, Vale WW The structures of the mouse and human urocortin genes (Ucn and UCN). Genomics 1998 May 15:50(1) :23-33
43． Joseph SA, Pilcher WH, Knigge KM. Anatomy of the corticotropin-releasing factor and opiomelanocortin systems of the brain. Fed Proc 1985 Jan;44(l Pt 1) : 100-7
44． Magiakou-MA; Mastorakos-G; Rabin-D; Dubbert-B; Gold-PW; Chrousos-GP Hypothalamic corticotropin-releasing hormone suppression during the postpartum period: implications for the increase in psychiatric manifestations at this time. J-Clin-Endocrinol-Metab. 1996 May; 81(5) : 1912-7
45． Muglia-LJ; Jacobson-L; Luedke-C; Vogt-SK; Schaefer-ML; Dikkes-P; Fukuda-S; Sakai-Y; Suda-T; Majzoub-JA Corticotropin-releasing hormone links pituitary adrenocorticotropin gene expression and release during adrenal insufficiencym J-Clin-Invest. 2000 May; 105(9) : 1269-77
46． Dijkstra-I; Tilders-FJ; Aguilera-G; Kiss-A; Rabadan-Diehl-C; Barden-N; Karanth-S; Holsboer-F; Reul-JM Reduced activity of hypothalamic corticotropin-releasing hormone neurons in transgenic mice with impaired glucocorticoid receptor function. J-Neurosci. 1998 May 15; 18(10) : 3909-18
47． Hucks D, Lowther S, Crompton MR, Katona CL, Morton RW, Corticotropin-releasing factor binding sites in cortex of depressed
suicides. Psychopharmacology (Berl). 1997 Nov;134(2) :174-8．
48． Yalow RS, Berson SA. Size heterogeneity of immunoreactive human ACTH in plasma and in extracts of pituitary glands and ACTH-producing thymoma. Biochem Biophys Res Commun 1971 Jul 16;44(2) :439-45
49． Lacroix M, Hontela A. Regulation of acute cortisol synthesis by cAMP-dependent protein kinase and protein kinase C in a teleost species, the rainbow trout (Oncorhynchus mykiss). J Endocrinol. 2001 Apr; 169(1) : 71-8．
50． Phillipov-G Effect of hypercortisolism and ACTH on the metabolism of cortisol. Exp-Clin-Endocrinol-Diabetes. 1998; 106(1) : 57-60
51． Rupprecht-R; Barocka-A; Pichl-J Correlations between clinico-psychiatric findings and the dexamethasone suppression test in depression Psychiatr-Prax. 1988 Jul; 15(4) : 142-5
52． Tatemoto-K; Efendic-S; Mutt-V; Makk-G; Feistner-GJ; Barchas-JD Pancreastatin, a novel pancreatic peptide that inhibits insulin secretion. Nature. 1986 Dec 4-10; 324(6096) : 476-8
53． Sauer-Ramirez-JL; Ballesteros-LM; Hernandez-Perez-O Galanin, a new neuropeptide. Review Ginecol-Obstet-Mex. 1996 Jul; 64: 325-31
54． Weiss JM, Bonsall RW, Demetrikopoulos MK, Emery MS, West CH. Galanin: a significant role in depression? Ann N Y Acad Sci 1998 Dec 21:863:364-82
55． Iismaa-TP; Shine-J Galanin and galanin receptors Results-Probl-Cell-Differ. 1999; 26: 257-91
56． lismaa-TP; Shine-J Galanin and galanin receptors Results-Probl-Cell-Differ. 1999; 26: 257-91
57． Weiss-JM; Bonsall-RW; Demetrikopoulos-MK; Emery-MS; West-CH Galanin: a significant role in depression? Ann-N-Y-Acad-Sci. 1998 Dec 21; 863: 364-82
58． Sauer-Ramirez-JL; Ballesteros-LM; Hernandez-Perez-O Galanin,
a new neuropeptide. Review Ginecol-Obstet-Mex. 1996 Jul; 64: 325-31
59． Weiss JM, Bonsa11 RW, Demetrikopoulos MK, Emery MS, West CH. Galanin: a significant role in depression? Ann N Y Acad Sci 1998 Dec 21:863:364-82
60． Cross-LJ; Beck-Sickinger-AG; Bienert-M; Gaida-W; Jung-G; Krause-E; Ennis-M Structure activity studies of mast cell activation and hypotension induced by neuropeptide Y (NPY), centrally truncated and C-terminal NPY analogues. Br-J-Pharmacol. 1996 Jan; 117(2) : 325-32
61． Graf-AH; Hutter-W; Hacker-GW; Steiner-H; Anderson-V; Staudach-A; Dietze-0 Localization and distribution of vasoactive neuropeptides in the human placenta. Placenta. 1996 Sep; 17(7) : 413-21
62． Higuchi-H Physiological functions of neuropeptide Y (NPY) and its gene expression Tanpakushitsu-Kakusan-Koso. 1997 May; 42(6) : 812-24
63． Widerlov-E; Lindstrom-LH; Wahlestedt-C; Ekman-R Neuropeptide Y and peptide YY as possible cerebrospinal fluid markers for major depression and schizophrenia, respectively. J-Psychiatr-Res. 1988; 22(1) : 69-79
64． Ekstrom-J; Brodin-E; Ekman-R; Hakanson-R; Sundler-F Vasoactive intestinal peptide and substance P in salivary glands of the rat following denervation or duct ligation Regul-Pept. 1984 Dec; 10(1) : 1-10
65． Berrettini-WH; Nurnberger-JI Jr; DiMaggio-DA Neuropeptide Y immunoreactivity in human cerebrospinal fluid. Peptides. 1986 May-Jun; 7(3) : 455-8
66． Caberlotto L, Jimenez P, Overstreet DH, Hurd YL, Mathe AA, Fuxe K. Alterations in neuropeptide Y levels and Y1 binding sites in the Flinders Sensitive Line rats, a genetic animal model of depression. Neurosci Lett 1999 Apr 23;265(3) :191-4
67． Melanie D. Mark, Stefan Herlitze. G-protein mediated gating of
inward rectifer K+ channels . Eur. J. Biochem, 2000:267:5830-5836
68． Nathan Dascal. Signalling Via the G Protein-Activated K+ Channels Cell. Signal, 1997 ;9(8) :551-573 .
69． Diomedes E. Logothetis, Yoshihisa Kurachi, Jonas Galper et al. The β γ subunits of GTP binding proteins activate the muscarinic K+ channels in heart. Nature, 1987:325(2) :321-326
70． Shojiro Isomot, Chikako Kondo, Yoshikisa Kurachi et al. Inwardly rectifying potassium channels: their molecular heterogeneitity and function . Japanse Journal of Physiology, 1997:47(11-39)
71． Melanie D. Mark, Stefan Herlitze. G-protein mediated gating of inward rectifer K+ channels . Eur. J. Biochem, 2000:267:5830-5836
72． Melanie D. Mark, Stefan Herlitze. G-protein mediated gating of inward rectifer K+ channels . Eur. J. Biochem, 2000:267:5830-5836
73． Christine Karschin, Eike Dibmann, Walter Stuhmer et. al . GIRK(1-3) and GIRK(1-4) inwardly rectifying K+ channel mRNAs are differentially expressed in the rat brain. J. Neurosci, 1996;16(1) :3559-3570
74． Y. JoyceLiao, YuhNungJan, and Lily Yeh Jan Heteromutimerization of G-protein gated inwardly rectifying K+ channel proteins GIRK1 and GIRK2 and their expression inweaver brain . J. Neurosci, 1996;16(22) :7137-7150
75． Cheng He, Hailin Zhang, Tooraj Mirshahi et al . Identification of a potassium channel site that interacts with G protein subunits to agonist-induced signaling. Journal of Biological Chemistry, 1999;274(4) :12517-12524
76． Velmirovic B. M., Koyano K, Nakajima S. et al, Oppposing mechanisms of regulation of a G-protein-coupled inward rectifer K+ channels in rat brain neurons Proc. Natl. Acad. Sci.USA, 1995; 92(4) : 1590-1594．
77． 王雪琦,路长林,李丽云等,大鼠抑郁模型的脑核磁共振成象研究。中
华精神科杂志1999，32(1)：12-14
78．王雪琦，路长林，孙学军等，大鼠抑郁症模型脑磁共振成象和波谱研究。神经科学1999，15(2)：162-165
79．严进，路长林，王雪琦等，睫状神经营养因子对应激引起海马CA3神经元损害的作用。解剖学杂志，1999，22(2)：99-103
80．严进，路长林，何成，王雪琦等，睫状神经营养因子对应激引起行为障碍的作用。中国行为医学科学，2000，9(2)：81-83
81．严进，路长林，汤淑萍，何成，王成海，王雪琦等，CNTF对应激大鼠行为障碍和海马CA1神经元损害的作用，心理学报，2000，32(2)：210-216
82. Nancy A. Muma, Sheryl G. Beck Corticosteroids alter G protein inwardly rectifying potassium channels protein levels in hippocampal subfields Brain Research 839(1999) 331-335