<p>During adolescence, the Central Nervous System (CNS) undergoes key developmental processes, making it vulnerable to exogenous agents. Ethanol (EtOH) consumption and exposure to noise, common in human adolescent environments, have been linked to behavioral alterations. The hippocampus (HC) and the cerebellum (CE), key CNS regions involved in behavior regulation, are affected by these stimuli, though the mechanisms remain unclear. This study evaluated the effects of short-term voluntary EtOH consumption, alone or combined with noise exposure, on aminoacidergic neurotransmission and thioredoxin-1 (Trx-1) levels in the HC and CE of adolescent male rats. Male Wistar rats (28&#xa0;days old) were exposed to noise and subjected to a two-bottle free-choice EtOH intake paradigm for three days. Subsequently, levels of excitatory amino acid transporter 1 (EAAT-1), glutamate decarboxylase (GAD), and Trx-1 were measured in HC and CE. Results showed that exposure to EtOH or noise increased EAAT-1 multimers and decreased glycosylated EAAT-1 in the CE, whereas EtOH intake caused opposite effects in the HC. Additionally, both stimuli increased GAD levels and decreased Trx-1 in the HC, while ETOH intake increased Trx-1 levels only in the CE. No significant changes were observed when stimuli were combined. In summary, brief exposure to noise and/or EtOH during adolescence induced specific changes in neurotransmission and oxidative markers in HC and CE, potentially contributing to behavioral alterations. These findings suggest that even transient exposure can disrupt protective mechanisms against oxidative stress and excitotoxicity. This study provides insight into how adolescent environmental stressors may compromise CNS development and resilience.</p>