Ethanol Consumption in Mice Lacking CD14, TLR2, TLR4, or MyD88.

ABSTRACT:

Background

Molecular and behavioral studies support a role for innate immune proinflammatory pathways in mediating the effects of alcohol. Increased levels of Toll-like receptors (TLRs) have been observed in animal models of alcohol consumption and in human alcoholics, and many of these TLRs signal via the MyD88-dependent pathway. We hypothesized that this pathway is involved in alcohol drinking and examined some of its key signaling components.

Methods

Different ethanol (EtOH)-drinking paradigms were studied in male and female control C57BL/6J mice versus mice lacking CD14, TLR2, TLR4 (C57BL/10ScN), or MyD88. We studied continuous and intermittent access 2-bottle choice (2BC) and 1-bottle and 2BC drinking-in-the-dark (DID) tests as well as preference for saccharin, quinine,

SUBMITTER: Blednov YA 

PROVIDER: S-EPMC5332291 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature