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MORE THAN MICROGLIAL DEPLETION：PLX5622 ACTIVATES THE HEPATIC CONSTITUTIVE ANDROSTANE RECEPTOR TO ALTER ANESTHESIA AND ADDICTION
Kelei Caoand 3 co-authors
Shanghai Jiao Tong University School of Medicine
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS01-07AM-121
Presentation
Date TBA
Board: PS01-07AM-121
Event Information
Poster Board
PS01-07AM-121
Poster
View posterAbstract
The colony-stimulating factor 1 receptor (CSF1R) inhibitor, PLX5622, has been widely used to deplete microglia for functional characterization and therapeutic support. While diverse outcomes have been described after PLX5622 treatment, whether these phenotypes solely reflect microglial functions remain to be determined. Here, we show that transgenic microglial depletion did not mimic the accelerated anesthetic arousal and alleviated nicotine addiction withdrawal symptoms, observed after PLX5622 treatment in mice. We further identify that PLX5622 potently activates the mouse constitutive androstane receptor (CAR), leading to prominent induction of hepatic enzymes. Induced enzymatic activity enhances metabolism and clearance of anesthetics and nicotine, thereby contributing to anesthetic insensitivity and addiction relief. Inactivation of CAR abolished these effects of PLX5622, indicating that the impacts of PLX5622 treatment cannot be attributed exclusively to microglial depletion. Our findings raise awareness in evaluating consequences of PLX5622 treatment and present insights into the design of specific CSF1R inhibitors.
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