Skip to main content
. 2015 Mar 31;9:40. doi: 10.3389/fncel.2015.00040

Figure 1.

Figure 1

Schematic rappresentation of the direct and indirect effect of stress on inflammation and neuroplasticity related processes. Stress induces directly an immediate release of glucocorticoids and pro-inflammatory cytokines (IL-1β, IL-6, CRP, TNF-α, INF-α); in turn incresead levels of glucocorticoids act on the brain by altering the CRH-ACTH signaling and, in turn, negatively affecting neurogenesis as well as the production of neurotrophic factors, including Brain Derived neurotrophic Factor (BDNF). Similarly, proinflammatory cytokines can negatively affect brain functioning and neurotrophins production and release. Stress can also work indirectly by activating epigenetic mechanisms (methylation, deacetylation, miRNAs), which may act on the same target stress related genes i.e., glucocorticid receptors, cytokines and BDNF. Red arrows indicate a suppressive effect, green arrows a stimulating effect.