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Developmental exposure to manganese induces lasting motor and cognitive impairment in rats
Tanara V Peres1, Helena Eyng2, Samantha C Lopes3
1Programa de Pós-graduação em Neurociências, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, Florianópolis, SC, Brazil.
Abstract:
Exposure to high manganese (Mn) levels may damage the basal ganglia, leading to a syndrome analogous to Parkinson's disease, with motor and cognitive impairments. The molecular mechanisms underlying Mn neurotoxicity, particularly during development, still deserve further investigation. Herein, we addressed whether early-life Mn exposure affects motor coordination and cognitive function in adulthood and potential underlying mechanisms. Male Wistar rats were exposed intraperitoneally to saline (control) or MnCl2 (5, 10 or 20 mg/kg/day) from post-natal day (PND) 8-12. Behavioral tests were performed on PND 60-65 and biochemical analysis in the striatum and hippocampus were performed on PND14 or PND70. Rats exposed to Mn (10 and 20 mg/kg) performed significantly worse on the rotarod test than controls indicating motor coordination and balance impairments. The object and social recognition tasks were used to evaluate short-term memory. Rats exposed to the highest Mn dose failed to recognize a familiar object when replaced by a novel object as well as to recognize a familiar juvenile rat after a short period of time. However, Mn did not alter olfactory discrimination ability. In addition, Mn-treated rats displayed decreased levels of non-protein thiols (e.g. glutathione) and increased levels of glial fibrillary acidic protein (GFAP) in the striatum. Moreover, Mn significantly increased hippocampal glutathione peroxidase (GPx) activity. These findings demonstrate that acute low-level exposure to Mn during a critical neurodevelopmental period causes cognitive and motor dysfunctions that last into adulthood, that are accompanied by alterations in antioxidant defense system in both the hippocampus and striatum.
Insights
Early-life exposure to manganese (Mn) in rats caused lasting motor and cognitive deficits into adulthood. This neurotoxicity was linked to altered antioxidant defenses in the brain, highlighting developmental risks.
Area of Science:
- Neuroscience
- Toxicology
- Developmental Biology
Background:
- High manganese (Mn) exposure can lead to basal ganglia damage, mimicking Parkinson's disease symptoms.
- The precise molecular mechanisms of Mn neurotoxicity during development require further exploration.
Purpose of the Study:
- To investigate the long-term effects of early-life manganese exposure on motor coordination and cognitive function in adult rats.
- To explore the underlying biochemical mechanisms, including alterations in the antioxidant defense system.
Main Methods:
- Wistar rats were exposed to manganese chloride (MnCl2) or saline from post-natal day 8-12.
- Behavioral assessments (rotarod, object recognition, social recognition) were conducted in adulthood.
- Biochemical analyses of striatum and hippocampus were performed to measure glutathione, GFAP, and GPx activity.
Main Results:
- Manganese exposure (10 and 20 mg/kg) significantly impaired motor coordination and balance in the rotarod test.
- High-dose Mn exposure resulted in deficits in object and social recognition, indicating memory impairment.
- Neurochemical analysis revealed decreased non-protein thiols and increased GFAP in the striatum, and increased GPx activity in the hippocampus.
Conclusions:
- Acute, low-level manganese exposure during a critical neurodevelopmental window induces persistent motor and cognitive impairments.
- These functional deficits are associated with disruptions in the antioxidant defense system in the hippocampus and striatum.
- The findings underscore the neurodevelopmental risks associated with manganese exposure.
