Genomic mechanisms of anxiety and depression pathogenesis in experimental models

• Published in: Obozrenie psikhiatrii i medit︠s︡inskoĭ psikhologii imeni V.M. Bekhtereva no. 4-1; pp. 48 - 50
• Main Authors: Kalueff, A. V., Demin, K. A., Volgin, A. D.
• Format: Journal Article
• Language: English
• Published: Federal State Budget Scientific Institution National Medical Research Center for Psychiatry and Neurology n.a. V.M. Bekhterev Ministry of Health of the Russian Federation 09.12.2019
• Subjects: genomic responses, stress, experimental models, mice, anxiety and depression
• ISSN: 2313-7053; 2713-055X
• DOI: 10.31363/2313-7053-2019-4-1-48-50

Affective disorders — including anxiety and depression — are the most prevalent human brain diseases. Stress is the most common cause of these human psychopathologies, and is also often used to develop their experimental models in animals. In addition to genetic and environmental factors, genomic and epigenetic processes play an important role in affective pathogenesis. The aim of the present study is to examine the expression of brain genes in mice in the chronic 20-day social stress model developed by Prof. N.N. Kudryavtseva (Institute of Cytology and Genetics) and to experimentally test the hypothesis on ‘genes-integrators’ whose brain activity can specifically integrate anxiety-depressive mechanisms. The report will for the first time provide data on the existence of several such putative brain genes whose expression in the hippocampus and cortex changes dynamically as stress transitions from the «anxiety» (10 days) to the «depressive» phase (20 days), including a number of cytokine and cellular structural genes whose expression is specifically altered only in the «transitional» stage (15 days). The findings provide a new perspective on the complex genomics of the anxiety-depressive pathogenesis of the CNS, and can be translationally significant, including in terms of finding new potential targets for the therapy of anxiety and depression based on such ‘gene-integrators’.