DOI: 10.1101/476457Nov 21, 2018Paper

Toll-like receptor 3 activation increases voluntary alcohol intake in C57BL/6J male mice

BioRxiv : the Preprint Server for Biology
Anna S WardenR Adron Harris

Abstract

Many genes differentially expressed in brain tissue from human alcoholics and animals that have consumed large amounts of alcohol are components of the innate immune toll-like receptor (TLR) pathway. TLRs initiate inflammatory responses via two branches: (1) MyD88-dependent or (2) TRIF-dependent. All TLRs signal through MyD88 except TLR3. Prior work demonstrated a direct role for MyD88-dependent signaling in regulation of alcohol consumption. However, the role of TLR3 as a potential regulator of excessive alcohol drinking has not previously been investigated. To test the possibility TLR3 activation regulates alcohol consumption, we injected mice with the TLR3 agonist polyinosinic:polycytidylic acid (poly(I:C)) and tested alcohol consumption in an every-other-day two-bottle choice test. Poly(I:C) produced a persistent increase in alcohol intake that developed over several days. Repeated poly(I:C) and ethanol exposure altered innate immune transcript abundance; increased levels of TRIF-dependent pathway components correlated with increased alcohol consumption. Administration of poly(I:C) before exposure to alcohol did not alter alcohol intake, suggesting that poly(I:C) and ethanol must be present together to change drinking behav...Continue Reading

Related Concepts

Ethanol
Genes
Laboratory mice
Poly I-C
EIF-2 Kinase
Branching (Qualifier Value)
Agonists
Brain Tissue
Toll-like receptors
Gene Mutant

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