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Rationale Exposure to social defeat (SD) induces a depressive phenotype, increased ethanol seeking and consumption, accompanied by activation of the neuroinflammatory response. However, a resilient response can be potentiated through physical exercise in the form of voluntary wheel running (VWR) during or after exposure to social stress. Therefore, the aim of this study was to test whether physical exercise during adolescence prior to being exposed to SD can enhance resilience to the increase in ethanol intake. Methods Male mice had access to VWR during adolescence and the effects of social defeat (4 sessions every 72 h) on oral ethanol self-administration (SA) was evaluated. Based on the social interaction test, mice were classified as resilient or susceptible to depressive-like behavior. Two weeks after the last encounter, mice were subjected to the drinking in the dark and oral ethanol SA paradigms. Mice were then sacrificed to measure brain-derived neurotrophic factor (BDNF) levels in the striatum and hippocampus. Results As expected, susceptible mice increased ethanol intake in the oral SA protocol. However, susceptible mice in the exercise condition did not increase ethanol intake, showing similar consumption and motivation for ethanol than the control and resilient groups. On the other hand, decreased BDNF levels were observed in susceptible mice in both experimental conditions compared to the control groups after ethanol SA. Conclusions The pre-exposure of VWR prevented the increase in consumption and motivation for ethanol induced by SD in susceptible mice. On the other hand, it appears that VWR did not exhibit any significant long-term effects on BDNF signaling, which is mainly affected in susceptible mice after ethanol intake.
Rationale Exposure to social defeat (SD) induces a depressive phenotype, increased ethanol seeking and consumption, accompanied by activation of the neuroinflammatory response. However, a resilient response can be potentiated through physical exercise in the form of voluntary wheel running (VWR) during or after exposure to social stress. Therefore, the aim of this study was to test whether physical exercise during adolescence prior to being exposed to SD can enhance resilience to the increase in ethanol intake. Methods Male mice had access to VWR during adolescence and the effects of social defeat (4 sessions every 72 h) on oral ethanol self-administration (SA) was evaluated. Based on the social interaction test, mice were classified as resilient or susceptible to depressive-like behavior. Two weeks after the last encounter, mice were subjected to the drinking in the dark and oral ethanol SA paradigms. Mice were then sacrificed to measure brain-derived neurotrophic factor (BDNF) levels in the striatum and hippocampus. Results As expected, susceptible mice increased ethanol intake in the oral SA protocol. However, susceptible mice in the exercise condition did not increase ethanol intake, showing similar consumption and motivation for ethanol than the control and resilient groups. On the other hand, decreased BDNF levels were observed in susceptible mice in both experimental conditions compared to the control groups after ethanol SA. Conclusions The pre-exposure of VWR prevented the increase in consumption and motivation for ethanol induced by SD in susceptible mice. On the other hand, it appears that VWR did not exhibit any significant long-term effects on BDNF signaling, which is mainly affected in susceptible mice after ethanol intake.
O estilo de vida desencadeia processos biológicos que levam o corpo a uma exaustão mista, levando a um estado chamado "stress", adoecendo ou agravando patologias. O objetivo deste estudo é analisar o estresse emocional sobre o sistema imunológico e desenvolver um conceito abrangente que permita menos ramificações errôneas em sua abordagem. Esta é uma revisão de literatura baseada em artigos em Imunologia retirados do banco de dados da PubMed. Foram selecionados artigos que relacionavam o problema de estresse com a etiologia imunopatogênica, publicados entre 2021 e 2022 (até 16 de março de 2022) e pesquisados com os termos truncados "imunologia do estresse", "fisiologia do estresse" e "psicologia do estresse". Evidenciamos que o estresse emocional é multifacetado, muda de acordo com a natureza do estímulo, pode ser benigno ou deletério e pode afetar populações de TCDs, que começam a carregar "cicatrizes" que as tornam hiper-responsivas a atividades inflamatórias em células-tronco, células B e NK. Moléculas como mTOR e PI3K, que expõem agentes virais dos APCs, levam à escassez do processo. Em uma situação contrária ao estresse, as citocinas pró-inflamatórias TNF-α tendem a se equilibrar, melhorando o tratamento com noxa. O estresse pode agravar inúmeras condições nos sistemas biológicos. Entretanto, o estresse "positivo" é responsável pelo aprendizado, tornando o processo alostático menos dispendioso. A condição cognitiva e a natureza estressante podem influenciar uma melhor reatividade e aprendizagem. Descobrimos que o estresse negativo que eleva os níveis de glicocorticóides é cognitivo-dependente, prevendo o agravamento de patologias crônicas ou produzindo seqüelas. Finalmente, concluímos que o estresse é todo causa e efeito exógeno que fisiologicamente são desencadeadores neuroimunoendócrinos da resposta cognitivo-dependente, o que leva o sistema à homeostase por natureza, independentemente da causa de seus danos, seja ela benigna e/ou deletéria, na forma aguda de caráter bioinformacional e na forma imunopatogênica crônica.
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