No abstract

Sepsis is defined as the host's reaction to infection and it is characterized by a systemic inflammatory response with important clinical implications. Central nervous system dysfunction secondary to sepsis is associated with local generation of pro- and anti-inflammatory cytokines, impaired cerebral microcirculation, disturbance of neurotransmitters, apoptosis, and cognitive impairment. It is known that during the process of learning and memory formation several pathways are involved such as dopaminergic and cholinergic systems. Thus, the objective of this study is to evaluate the neuronal calcium sensor (NCS-1) and dopamine-cAMP regulated phosphoprotein of 32,000 kDa (DARPP-32) expression as well as brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) levels in prefrontal cortex and hippocampus of rats 12, 24, and 48 h after sepsis induction. To this aim, we used sham-operated Wistar rats or submitted to the cecal ligation and perforation procedure. After 12 and 24 h, there was an increase of NGF levels in hippocampus; and up to 48 h, a decrease of NCS-1 expression in prefrontal cortex, a decrease of BDNF levels in hippocampus and an increase of NGF levels in hippocampus. In conclusion, we believe that the low expression of NCS-1 in prefrontal cortex and low levels of BDNF in hippocampus may be associated with the pathophysiology of cognitive impairment during sepsis and a putative role of the dopaminergic system.

No abstract

The systemic inflammation that occurs during severe sepsis can be the cause of long-term consequences. Studies have demonstrated a possible correlation between the neuroinflammatory process and depression. However, the effects of mild sepsis as a tolerant factor for some depressive parameters have not been described. Thus, the objective of this study is to evaluate the effect of mild sepsis on behavioral and biochemical changes on the stress-induced animal model of depression. To this aim, adult male Wistar rats were submitted to cecal ligation and perforation and after 30 days it was submitted to the chronic mild stress protocol (CMS). The animals were submitted to stressors for 40 days. To evaluate the efficacy of CMS induction anhedonia was determined as the amount of sweet food consumption. The levels of neurotrophins and oxidative damage were also evaluated in the hippocampus. It is observed that mild sepsis improved depressive-like parameters after CMS protocol associated with an increase of neurotrophins levels and a decrease of oxidative damage in the hippocampus. In conclusion, our data suggest that a previous mild systemic inflammation caused by the induction of mild sepsis could decrease consequences in the central nervous system (CNS) induced by CMS protocol.