Zinc Alleviates Lipopolysaccharide Interference with Both Body Temperature and Sickness Behavior in Virgin Female Rats

Abstract

Objectives: Previous studies from our group showed that lipopolysaccharide (LPS) exposure induces several signs of sickness behavior, including a decrease in food consumption, body weight gain, adipsia, and a biphasic effect in tympanic temperature with a first phase of hypothermia, followed by an increased tympanic temperature. LPS can activate a chain of nonspecific host responses, including the immune response, and decreased zinc levels. In addition, there are differences in the immune response between males and females, particularly fever, with sex hormones interfering with body temperature. This study aims to characterize the effects of zinc treatment on tympanic temperature, body weight gain, food and water consumption, and general activity in open field of virgin female rats exposed to a dose of LPS that was previously reported to induce sickness behavior. Methods: Virgin female Wistar rats were treated with either saline (S) or LPS. One hour later, the S group received another injection of saline (S + S group), half of the LPS group received saline (LPS + S group) and the other half received zinc (LPS + Zn group). Tympanic temperature, body weight, and water and food consumption were measured for 96 h. Measurements and observations started 2 h after LPS administration. Results: Treatment with zinc attenuated LPS-increased temperature, decreased the body weight gain and food consumption, and water consumption was increased. Conclusion: Zinc treatment is beneficial as it reduces the increased tympanic temperature induced by LPS, but it does not influence other sickness behavior caused by exposure to LPS.

Antidepressant effect of PT-31, an α₂-adrenoceptor agonist, on lipopolysaccharide-induced depressive-like behavior in mice

“…Lipopolysaccharide is widely used to induce behavioral changes in rodents through neuroinflammation (Müller et al ., 2015; Domingues et al ., 2018; Lee et al ., 2020). Initially, lipopolysaccharide activates Toll-like receptors 4 (TLR4) and nuclear translocation of nuclear factor-κB (NF-κB), which leads to the release of TNF-α, IL-1β, and IL-6 2 h after lipopolysaccharide administration (Nascimento et al ., 2018b; Gomes et al ., 2020). These peripheral cytokines induce the synthesis of cytokines in the central nervous system (CNS) by microglia, affecting serotonergic and glutamatergic neurotransmission, and resulting in sickness behavior 6 h postlipopolysaccharide (Zhao et al ., 2019).…”