Myeloid differentiation primary response protein (MyD88) is a critical neuroimmune adaptor protein in TLR (Toll-like receptor) and IL-1R (Interleukin-1 receptor) signaling complexes. These two pro-inflammatory families play an important role in the neurobiology of alcohol use disorder, specifically MyD88 regulates ethanol drinking, ethanol-induced sedation, and ethanol-induced deficits in motor coordination. In this study, we examined the role of MyD88 in mediating the effects of IL-1β and ethanol on GABAergic transmission in the central amygdala (CeA) of male mice using whole-cell patch-clamp recordings in combination with pharmacological (AS-1, a mimetic that prevents MyD88 recruitment by IL-1R) and genetic ( knockout mice) approaches. We demonstrate through both approaches that IL-1β and ethanol's modulatory effects at CeA GABA synapses are not dependent on MyD88. knockout potentiated IL-1β's actions in reducing postsynaptic GABA receptor function. Pharmacological inhibition of MyD88 modulates IL-1β's action at CeA GABA synapses similar to knockout mice. Additionally, ethanol-induced CeA GABA release was greater in knockout mice compared to wildtype controls. Thus, MyD88 is not essential to IL-1β or ethanol regulation of CeA GABA synapses but plays a role in modulating the magnitude of their effects, which may be a potential mechanism by which it regulates ethanol-related behaviors.
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| http://dx.doi.org/10.3390/brainsci9120361 | DOI Listing |
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