scholarly journals Summary of a National Institute of Mental Health workshop: developing animal models of anxiety disorders

2001 ◽  
Vol 157 (4) ◽  
pp. 327-339 ◽  
Author(s):  
Shekhar A. ◽  
McCann U. ◽  
Meaney M. ◽  
Blanchard D. ◽  
Davis M. ◽  
...  
2011 ◽  
pp. 156-167 ◽  
Author(s):  
Jesse W. Richardson-Jones ◽  
E. David Leonardo ◽  
Rene Hen ◽  
Susanne E. Ahmari

2013 ◽  
Vol 35 (suppl 2) ◽  
pp. S101-S111 ◽  
Author(s):  
Alline C. Campos ◽  
Manoela V. Fogaca ◽  
Daniele C. Aguiar ◽  
Francisco S. Guimaraes

Author(s):  
Richard McCarty

Much of the research relating to animal models of anxiety has been devoted to developing more effective drugs for the treatment of the various anxiety disorders. Using selective breeding of laboratory mice and rats, investigators have developed high-anxiety and low-anxiety lines that have been especially valuable for basic research purposes. Other approaches to enhance the expression of an anxiety-like phenotype have included prenatal or early postnatal exposure to stressors, maternal immune activation, or selecting offspring based upon differences in the maternal behaviors of their mothers. In addition, risk genes for anxiety disorders have been studied in animal models, including genes related to serotonin, neuropeptide Y, neuropeptide S, and corticotropin-releasing factor signaling in the brain. Finally, some infant rhesus monkeys display an anxious temperament and extreme behavioral inhibition when separated from their mothers. This nonhuman primate model affords many opportunities to explore brain mechanisms and interventions that may be effective in preventing the further development of an anxious phenotype as these monkeys mature.


CNS Spectrums ◽  
2001 ◽  
Vol 6 (7) ◽  
pp. 590-594 ◽  
Author(s):  
Florian Holsboer

AbstractResearch has provided considerable evidence for the hypothesis that corticotropin-releasing hormone (CRH), the key central coordinator of stress-hormone homeostasis, also plays a role in the development and course of depression and anxiety disorders. Studies using animal models of anxiety, as well as mouse mutants, in which the gene coding for the CRH type 1 receptor (CRHR1) was genetically deleted supported the notion that enhanced CRH/CRHR1 signaling underlies depression and anxiety disorders. Therefore, a number of small nonpeptide molecules that antagonize CRHR1 have been developed. In animal models, these molecules had anxiolytic and other stress-alleviating effects. An initial clinical study showed that CRHR1 antagonism has beneficial effects on depression and anxiety symptoms at doses unharmful to neuroendocrine stress responsivity.


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