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RESEARCH PRODUCT

Ethanol intake in male mice exposed to social defeat: Environmental enrichment potentiates resilience

Marta Rodríguez-ariasCarmen Ferrer-pérezMarina D. ReguilónJosé MiñarroCarmen Manzanedo

subject

Neurophysiology and neuropsychologymedicine.medical_specialtyChemokinePhysiologyNeurosciences. Biological psychiatry. NeuropsychiatryStriatumBiochemistrySocial defeatCellular and Molecular NeuroscienceEndocrinologyNeuroinflammationSocial defeatInternal medicinemedicineOriginal Research ArticlePrefrontal cortexCX3CL1RC346-429Molecular BiologyNeuroinflammationSocial stressEnvironmental enrichmentbiologyEthanolResilienceEndocrine and Autonomic Systemsbusiness.industryQP351-495Environmental enrichmentEndocrinologySusceptibilitybiology.proteinNeurology. Diseases of the nervous systembusinessRC321-571

description

Large preclinical evidence shows that exposure to social defeat (SD) increases vulnerability to drug abuse, increasing the consumption of ethanol. However, not all subjects are equally affected by the changes induced by stress. Previous reports have evidenced that the resilient phenotype to depressive-like behaviors after SD is associated with the resistant phenotype to cocaine-increased rewarding effects and the smaller neuroinflammatory response. The aim of the present study was to further clarify whether the resilient profile to depressive-like behavior also predicts a protection against the increase in ethanol intake induced by SD. The neuroinflammatory profile was studied after the end of the oral ethanol self-administration (SA) procedure, measuring levels of the pro-inflammatory cytokine IL-6 and the chemokine CX3CL1 or fractalkine in the striatum and prefrontal cortex. Previous studies have shown that environmental enrichment (EE) is an effective mechanism to dimish the detrimental effects of social stress. In a second study, we aimed to evaluate if EE housing before exposure to SD could potentiate resilience. Our results showed that mice with a phenotype susceptible to SD-induced depressive-like behaviors showed increased ethanol consumption and increased neuroinflammatory signaling. In contrast, despite the lack of effect on depressive-like behaviors, defeated mice previously housed under EE conditions did not show an increase in ethanol SA or an increase in immune response. To sum up, the resilient phenotype to SD develops at different levels, such as depressive-like behaviors, ethanol consumption and the neuroinflammatory response. Our results also point to the protective role of EE in potentiating resilience to SD effects.

10.1016/j.ynstr.2021.100413http://www.sciencedirect.com/science/article/pii/S2352289521001211