Chronic stress, together with ageing, is a major risk factor for the development of many brain disorders and diseases. Many of these disorders are characterized byinflammation activation, which is involved in both the insurgence and progression of neurodegenerative pathologies, such as Alzheimer and Parkinson’s disease. To study the relationship between chronic stress, inflam- mation and related diseases, rodent models are com- monly used. Models of stress include a variety of socially and physically stressful events that are carried out for a variable period of timein order to simulate either acute or chronic stress. The complexity and diversity of stress paradigms, i.e. the types and combinations of stress- ors, as well as the duration of the protocol,challenge the effectiveness and reproducibility of these models. There- fore, it’s critical to carry out the characterization of the models before investigating the role of inflammation and their relationship to chronic stress in humans. In the chronic stress model applied in this work mice were randomly assigned to control or stress group: animals of stress group were exposed every day for 24 weeks to a random chronic mild stress stimulus among Isolation, Social stress, Damp bedding, Removal of bedding, Cage tilting at 45°, Restraint Stress Loading, Alteration of light/dark cycle, Intermittent illumination, Food deprivation, Water deprivation, Tail Suspension Test, Forced swimming test. Inflammation activation was evaluated by GFAP and IBA1 expression; moreover, considering the known impact of stress on the synthesis and release of dopamine within mesocortical, mesoac- cumbens, and nigrostriatal dopamine projections, TH and DAT expression were evaluated. Preliminary results showed evidence of microglial cell activation follow- ing stress stimulus, as well as a slight decrease of DAT expression in the caudate putamen. Further studies are needed to measure the changes in specific inflammatory mediators, including NF-κB and TLRs, and inflamma- tory cytokines, such as TNF-α, IL-1β, and IL-6.
Characterization of a mouse model of chronic stress-induced neuroinflammation
Maria Antonietta Panaro;Antonia Cianciulli;Rosa Calvello;
2024-01-01
Abstract
Chronic stress, together with ageing, is a major risk factor for the development of many brain disorders and diseases. Many of these disorders are characterized byinflammation activation, which is involved in both the insurgence and progression of neurodegenerative pathologies, such as Alzheimer and Parkinson’s disease. To study the relationship between chronic stress, inflam- mation and related diseases, rodent models are com- monly used. Models of stress include a variety of socially and physically stressful events that are carried out for a variable period of timein order to simulate either acute or chronic stress. The complexity and diversity of stress paradigms, i.e. the types and combinations of stress- ors, as well as the duration of the protocol,challenge the effectiveness and reproducibility of these models. There- fore, it’s critical to carry out the characterization of the models before investigating the role of inflammation and their relationship to chronic stress in humans. In the chronic stress model applied in this work mice were randomly assigned to control or stress group: animals of stress group were exposed every day for 24 weeks to a random chronic mild stress stimulus among Isolation, Social stress, Damp bedding, Removal of bedding, Cage tilting at 45°, Restraint Stress Loading, Alteration of light/dark cycle, Intermittent illumination, Food deprivation, Water deprivation, Tail Suspension Test, Forced swimming test. Inflammation activation was evaluated by GFAP and IBA1 expression; moreover, considering the known impact of stress on the synthesis and release of dopamine within mesocortical, mesoac- cumbens, and nigrostriatal dopamine projections, TH and DAT expression were evaluated. Preliminary results showed evidence of microglial cell activation follow- ing stress stimulus, as well as a slight decrease of DAT expression in the caudate putamen. Further studies are needed to measure the changes in specific inflammatory mediators, including NF-κB and TLRs, and inflamma- tory cytokines, such as TNF-α, IL-1β, and IL-6.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
