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Olfactory dysfunction is a common outcome of brain injuries, negatively affecting quality of life. The adult mammalian nervous system has limited capacity for olfactory recovery, making it challenging to study olfactory regeneration and recovery. In contrast, zebrafish are ideal for such studies due to its extensive and lifelong regenerative abilities. In this work, we describe a model of excitotoxic injury in the olfactory bulb (OB) using quinolinic acid lesions in adult zebrafish of both sexes. We observed extensive neurodegeneration in both the OB and olfactory epithelium, including a reduction of bulbar volume, neuronal death, and impaired olfactory function. Recovery mechanisms involved tissue remodeling, cell proliferation, and neurogenesis, leading to full restoration of olfactory function by 21 d. This study provides a model to further investigate the effects of excitotoxicity on olfactory dysfunction and highlights zebrafish's remarkable regenerative abilities, providing insights into potential therapeutic strategies for restoring olfactory function following brain injuries.