Pain sensitization is a phenomenon that occurs to protect tissues from damage and recent studies have shown how a variety of non-noxious stimuli included in our everyday lives can lead to pain sensitization Consumption of large amounts of alcohol over a long period of time invokes alcohol use disorder (AUD), a complex pathological state that has many manifestations, including alcohol peripheral neuropathy (neuropathic pain). We asked if 'non-pathological' alcohol consumption can cause pain sensitization in the absence of other pathology? Studies have pointed to glia and other immune cells and their role in pain sensitization that results in cell and sex-specific responses (Wang et al., 2010; Obad et al., 2018). Using a low-dose and short-term ethanol exposure model, we investigated whether this exposure would sensitize mice to a subthreshold dose of an inflammatory mediator that normally does not induce pain, or cause hypersensitivity. We observed female mice exhibited specific mechanical and higher thermal sensitivity than males. We also observed an increase in CD68 macrophages in the ipsilateral dorsal root ganglia (DRG) and Iba1 microglia in the ipsilateral spinal dorsal horn of animals that were exposed to ethanol and injected with subthreshold prostaglandin E2. Our findings suggest that short-term ethanol exposure stimulates peripheral and central, immune, and glial activation, respectively to induce pain sensitization. This work begins to reveal a possible mechanism behind the development of alcoholic peripheral neuropathy.
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