C1q deletion exacerbates stress-induced learned helplessness behavior and induces neuroinflammation in mice.
Ontology highlight
ABSTRACT: Increased levels of pro-inflammatory cytokines have been reported in postmortem brain samples and in the blood of depressed subjects. However, the inflammatory pathways that lead to depressive-like symptoms are not well understood. Using the learned helplessness (LH) model of depression, we examined the role of C1q, the initiator of classical complement pathway in mediating stress-induced depressive-like behavior in mice. We observed no significant changes in social behavior, despair behavior, spatial memory, and aggressive behavior between the wild type (WT) and C1q knockout (KO) mice. However, C1q deletion exacerbated the inescapable electric foot shock-induced learned helplessness behavior in mice. We found significant reductions in C1q mRNA levels in the prefrontal cortex (PFC) of WT h
SUBMITTER: Madeshiya AK
PROVIDER: S-EPMC8807734 | biostudies-literature | 2022 Feb
REPOSITORIES: biostudies-literature
ACCESS DATA