Several studies implicate toll-like receptors (TLRs) in an alcohol-induced neuroinflammatory process.
The work conducted by Wu et al., and reported in this issue of the British Journal of Pharmacology indicates that TLR4 along with its intracellular adaptor protein-MyD88 may play crucial roles in the acute actions of alcohol.
The deletions of TLR4 or MyD88 gene or pharmacological inhibition of TLR4 by (+)-naloxone were able to attenuate alcohol-induced sedation, motor impairment, and acute alcohol-induced increases in IkBα protein levels in the hippocampus of mice.
These results clearly suggest that TLR4-MyD88 signaling may play a causal role in the mediation of the behavioral effects of acute alcohol.
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