Rats Selected for Different Nervous Excitability: Long-Term Emotional-Painful Stress Affects the Dynamics of DNA Damage in Cells of Several Brain Areas

被引:1
作者
Shcherbinina, Veronika [1 ,2 ]
Pavlova, Marina [1 ]
Daev, Eugene [1 ,2 ]
Dyuzhikova, Natalia [1 ]
机构
[1] Pavlov Inst Physiol, Russian Acad Sci, Lab Higher Nervous Act Genet, Nab Makarova 6, St Petersburg 199034, Russia
[2] St Petersburg State Univ, Fac Biol, Dept Genet & Biotechnol, Univ Skaya Nab 7-9, St Petersburg 199034, Russia
关键词
rats; stress; nervous system excitability; PTSD; compulsive disorder; DNA damage; comet assay; prefrontal cortex; hippocampus; amygdala; MECHANISMS;
D O I
10.3390/ijms25020994
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The maintenance of genome stability is critical for health, but during individual ontogenesis, different stressors affect DNA integrity, which can lead to functional and/or structural changes in the cells of target organs. In the nervous system, cell genome destabilization is associated with different neurological and psychiatric diseases, but experiments in vivo, where a link between stress and DNA instability has been demonstrated, are relatively rare. Here, we use rat strains selected for the contrast excitability of the tibialis nerve (n. tibialis) and nonselected Wistar rats to investigate the reasons for individual differences in developing post-stress pathologies. Previous research on the behavioral response of these strains to prolonged emotional-painful stress (PEPS) allows us to consider one strain as a model of post-traumatic stress disorder (PTSD) and another strain as a model of compulsive disorder (CD). We study DNA damage in the cells of the prefrontal cortex (PFC), hippocampus, and amygdala, regions involved in stress responses and the formation of post-stress dysfunctions. The evaluation of cell genome integrity via the comet assay shows different responses to PEPS in each brain area analyzed and for all strains used. This could help us to understand the reasons for individual differences in the consequences of stress and the pathophysiology of post-stress disease formation.
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页数:11
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