Imipramine reverses depressive-like parameters in pneumococcal meningitis survivor rats

Abstract

Pneumococcal meningitis is a severe infectious disease of the central nervous system, associated with acute inflammation and might cause damage to the host, such as deafness, blindness, seizure, and learning deficits. However, infectious diseases can play a significant role in the etiology of neuropsychiatric disturbances. In this context, we evaluated depressive-like parameters; corticosterone and ACTH levels in pneumococcal meningitis surviving rats. Wistar rats underwent a magna cistern tap receiving either 10 μL sterile saline or a Streptococcus pneumoniae suspension at the concentration of 5 × 10(9) cfu/mL. After 3 days of meningitis induction procedure, the animals were treated with imipramine at 10 mg/kg or saline for 14 days (3rd-17th day). The consumption of sweet food was measured for 7 days (10th-17th day). The meningitis group decreased the sucrose intake and increased the levels of corticosterone and ACTH levels in the serum and TNF-α in the cortex; however, the treatment with imipramine reverted the reduction of sweet food consumption, normalized hormonal levels and TNF-α in the cortex. Our results supported the hypothesis that the pneumococcal meningitis surviving rats showed depressive-like behavior and alterations in the hypothalamus-pituitary-adrenal axis.

Receptor for Advanced Glycation End Products (RAGE) Mediates Cognitive Impairment Triggered by Pneumococcal Meningitis

“…Cytokines may play a significant role in the pathogenesis of bacterial meningitis, and proinflammatory cytokines such as TNF-α, IL-β, and IL-6 are associated with poor outcomes in bacterial meningitis. In this study, TNF-α and IL-β levels remained elevated in the PFC at 10 days after meningitis induction, corroborating our previous reports demonstrating that TNF-α levels remained higher after antibiotic treatment in the frontal cortex [29]; this increase was also associated with long-term cognitive impairment [6,16]. In an in vitro study, the interaction between RAGE and its ligands induced TNF-α, IL-6, IL-1, and iNOS expression in microglial cell culture [30], and this study demonstrated that blocking RAGE prevented an increase in the levels of these cytokines.…”

Synergistic Effects of Celecoxib and Bupropion in a Model of Chronic Inflammation-Related Depression in Mice

“…This data confirms the growing body of evidence demonstrating that mood disorders, such as MDD, can be triggered by inflammation [13,41,42]. A comprehensive literature search revealed that fluoxetine, bupropion, or imipramine, when tested at a range of doses similar to that used in our study did not evoke any change of locomotor activity in the open-field test [43,44]. This might rather support our conclusions, on the basis of TST and FST experimental paradigm.…”

FAT/CD36: A Major Regulator of Neuronal Fatty Acid Sensing and Energy Homeostasis in Rats and Mice

“…However, although they had no increase in the percent of total carcass adiposity (using five pad weights as surrogates), VMH CD36–depleted rats did have a 20% increase in feed efficiency, a 125 and 65% increase in plasma leptin levels after 6 weeks of chow and 9 weeks of HFD, and a 60% increase in inguinal fat pad weights relative to carcass weights terminally. These differences from control rats suggest that VMH CD36–depleted rats had a redistribution of fat from visceral to subcutaneous (inguinal) depots, the predominant source of circulating leptin (32,33). Assuming this is so and that sparing of visceral depots by shunting fat to subcutaneous depots should improve insulin sensitivity, it was surprising to find that CD36 shRNA rats had markedly elevated plasma insulin levels and impaired glucose tolerance after both chow and HFD.…”