Cyp2e1 deletion in mice increases sensitivity to ethanol-induced motor impairment and escalation of drinking behavior in the chronic intermittent ethanol model.

ABSTRACT:

Background

Chronic ethanol use drives numerous neurological dysfunctions. Ethanol in the brain is mainly metabolized into acetaldehyde by catalase and cytochrome P450 2E1 (Cyp2e1), and acetaldehyde does not freely cross the blood-brain barrier. While Cyp2e1 is a well-known enzyme in liver toxicology, how central nervous system (CNS)-expressed Cyp2e1 contributes to ethanol toxicity is unknown.

Methods

We investigated the effects of Cyp2e1-driven ethanol metabolism in the brain of male and female global Cyp2e1 knockout (KO) and wild-type (WT) 129S1/SvImJ mice. RNA-seq was completed on the medial prefrontal cortex (mPFC), the dorsal and ventral hippocampus, and cerebellum to see whether there are baseline differences in gene expression between WT and KO mice. To investigate acu

SUBMITTER: Gonzalez HC 

PROVIDER: S-EPMC12721483 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature