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The herbicide 2,4-dichlorophenoxyacetic acid (2,4-D) is the second most widely used herbicide in the world. The objective of this study was to evaluate the neurotoxic effects and the possible role of the dysregulation of apoptosis in the genesis of brain damage in chronic exposure to 2,4-D in rats. Eighty adult male rats were distributed into eight groups (n = 10) and exposed orally (contaminated feed) and via inhalation, with two groups exposed to distilled water (control) and six to 2,4-D in three distinct concentrations. They were exposed for 6 months. A neurobehavioral assessment was performed, and the brain was collected for histopathology and immunohistochemistry. The animals in the control groups showed greater motility in the open-field test and a greater number of entries in the elevated-plus-maze test than those exposed to 2,4-D (p < 0.05). Neuronal necrosis was more incident in animals exposed to 2,4-D (p < 0.05). There was a negative correlation between the expression of BAX and the measurement of the cerebral cortex thickness (r = −0.713; p = 0.047). Regardless of the route of exposure, 2,4-D led to a deficit in neurobehavioral tests and decreased thickness of the cerebral cortex associated with increased expression of the pro-apoptotic protein BAX. [ABSTRACT FROM AUTHOR]