The contribution of an animal model toward uncovering biological risk factors for PTSD

被引:78
作者
Cohen, Hagit [1 ]
Matar, Michael A.
Richter-Levin, Gal
Zohar, Joseph
机构
[1] Ben Gurion Univ Negev, Fac Hlth Sci, Anxiety & Stress Res Unit, Minist Hlth,Mental Hlth Ctr, IL-84170 Beer Sheva, Israel
[2] Univ Haifa, Dept Psychol, IL-31905 Haifa, Israel
[3] Tel Aviv Univ, Sackler Sch Med, Chaim Sheba Med Ctr, IL-69978 Tel Aviv, Israel
来源
PSYCHOBIOLOGY OF POSTTRAUMATIC STRESS DISORDER: A DECADE OF PROGRESS | 2006年 / 1071卷
关键词
animal model; posttraumatic stress disorder; early-life stress; memory consolidation; anisomycin; hypothalamic-pituitary-adrenal (HPA) axis; selective serotonin reuptake inhibitors;
D O I
10.1196/annals.1364.026
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Clinical studies of posttraumatic stress disorder (PTSD) have elicited proposed risk factors for developing PTSD in the aftermath of stress exposure. Generally, these risk factors have arisen from retrospective analysis of premorbid characteristics of study populations. A valid animal model of PTSD can complement clinical studies and help to elucidate issues, such as the contribution of proposed risk factors, in ways which are not practicable in the clinical arena. Important qualities of animal models include the possibility to conduct controlled prospective studies, easy access to postmortem brains, and the availability of genetically manipulated subjects, which can be tailored to specific needs. When these qualities are further complemented by an approach which defines phenomenologic criteria to address the variance in individual response pattern and magnitude, enabling the animal subjects to be classified into definable groups for focused study, the model acquires added validity. This article presents an overview of a series of studies in such an animal model which examine the contribution of two proposed risk factors and the value of two early postexposure pharmacological manipulations on the prevalence rates of subjects displaying an extreme magnitude of behavioral response to a predator stress paradigm.
引用
收藏
页码:335 / 350
页数:16
相关论文
共 57 条
[1]   Low-dose cortisol for symptoms of posttraumatic stress disorder [J].
Aerni, A ;
Traber, R ;
Hock, C ;
Roozendaal, B ;
Schelling, G ;
Papassotiropoulos, A ;
Nitsch, RM ;
Schnyder, U ;
de Quervain, DJF .
AMERICAN JOURNAL OF PSYCHIATRY, 2004, 161 (08) :1488-1490
[2]   Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock [J].
Annane, D ;
Sébille, V ;
Charpentier, C ;
Bollaert, PE ;
François, B ;
Korach, JM ;
Capellier, G ;
Cohen, Y ;
Azoulay, E ;
Troché, G ;
Chaumet-Riffaut, P ;
Bellissant, E .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 2002, 288 (07) :862-871
[3]  
Annane D, 2002, CRIT CARE, V6, P190
[4]   Exposure to juvenile stress exacerbates the behavioural consequences of exposure to stress in the adult rat [J].
Avital, A ;
Richter-Levin, G .
INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY, 2005, 8 (02) :163-173
[5]   Plasma and cerebrospinal fluid interleukin-6 concentrations in posttraumatic stress disorder [J].
Baker, DG ;
Ekhator, NN ;
Kasckow, JW ;
Hill, KK ;
Zoumakis, E ;
Dashevsky, BA ;
Chrousos, GP ;
Geracioti, TD .
NEUROIMMUNOMODULATION, 2001, 9 (04) :209-217
[6]  
Bremner JD, 1997, AM J PSYCHIAT, V154, P624
[7]  
Breslau Naomi, 2002, Semin Clin Neuropsychiatry, V7, P80, DOI 10.1053/scnp.2002.31780
[8]   Stress doses of hydrocortisone reverse hyperdynamic septic shock: A prospective, randomized, double-blind, single-center study [J].
Briegel, J ;
Forst, H ;
Haller, M ;
Schelling, G ;
Kilger, E ;
Kuprat, G ;
Hemmer, B ;
Hummel, T ;
Lenhart, A ;
Heyduck, M ;
Stoll, C ;
Peter, K .
CRITICAL CARE MEDICINE, 1999, 27 (04) :723-732
[9]  
Bryant Richard A, 2005, J Trauma Dissociation, V6, P5, DOI 10.1300/J229v06n02_02
[10]   Variations in maternal care in infancy regulate the development of stress reactivity [J].
Caldji, C ;
Diorio, J ;
Meaney, MJ .
BIOLOGICAL PSYCHIATRY, 2000, 48 (12) :1164-1174