Microglia depletion fails to abrogate inflammation-induced sickness in mice and rats.

ABSTRACT:

Background

Production of inflammatory mediators by reactive microglial cells in the brain is generally considered the primary mechanism underlying the development of symptoms of sickness in response to systemic inflammation.

Methods

Depletion of microglia was achieved in C57BL/6 mice by chronic oral administration of PLX5622, a specific antagonist of colony stimulating factor-1 receptor, and in rats by a knock-in model in which the diphtheria toxin receptor was expressed under the control of the endogenous fractalkine receptor (CX3CR1) promoter sequence. After successful microglia depletion, mice and rats were injected with a sickness-inducing dose of lipopolysaccharide according to a 2 (depletion vs. control) × 2 (LPS vs. saline) factorial design. Sickness was measured by b

SUBMITTER: Vichaya EG 

PROVIDER: S-EPMC7262755 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature