Ethanol, a widely used toxic chemical in human cultures, exerts its toxicity throughout the human body, with the nervous system being particularly vulnerable, leading to various neurological disorders. Despite the prevalence of peripheral neuropathies associated with alcohol abuse, the causal mechanism of ethanol-induced peripheral neuropathies remains largely unknown. This study investigated the impact of repeated ethanol intake on the histological features of trigeminal ganglia in mice. Histological analysis revealed that blood vessels in the trigeminal ganglia exhibited distinct morphological and molecular characteristics based on their location, specifically in regions where neuronal cell bodies or axonal fibers predominate. Administration of a binge level of ethanol for four consecutive days induced significant blood vessel remodeling in both regions. Unexpectedly, the morphology of trigeminal neurons and their axons remained unaffected by ethanol. Given the observed suppression of IBA1/AIF1-positive microglia-like cells by ethanol, we explored whether manipulative suppression of microglia-like cell activity with minocycline could recapitulate ethanol-induced effects. Remarkably, administration of minocycline, instead of ethanol, resulted in similar blood vessel remodeling, suggesting that the repeated intake of a binge level of ethanol causes blood vessel remodeling through the suppression of microglia-like cells in the trigeminal ganglia. These findings provide valuable insights into the complex interplay between ethanol exposure, microglia-like cell activity, and vascular changes in the trigeminal ganglia.