Researchers administered 10 mg/kg polystyrene particles (0.5 or 1 μm) intraperitoneally to Sprague-Dawley rats, finding that larger 1 μm particles produced more severe neurological damage within 24 hours. The hippocampus showed the greatest vulnerability, with disrupted acetylcholinesterase activity and elevated oxidative stress markers, particularly in female subjects. Co-exposure with glyphosate created complex interaction patterns ranging from additive to antagonistic effects. This acute toxicity study provides concerning evidence that ubiquitous plastic pollutants can rapidly penetrate brain tissue and disrupt fundamental neurochemical processes. The findings extend beyond previous research focused on chronic exposure, demonstrating that even single encounters with microplastics at environmentally relevant concentrations can trigger measurable neurotoxicity. The sex-specific vulnerability patterns and regional brain differences suggest that plastic pollution may pose heterogeneous risks across populations. However, the intraperitoneal injection method bypasses natural exposure routes, potentially overestimating real-world effects. The 24-hour timeframe also leaves questions about recovery potential and long-term consequences. While this controlled study establishes biological plausibility for microplastic neurotoxicity, translating these findings to human health risks requires additional research examining realistic exposure pathways and chronic effects.