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Published on: June 17, 2015
Effects of methylmercury on postnatal neurobehavioral development in mice
1Environmental Health Department, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Abstract:
Eighty ICR mice were randomly assigned to one of four groups given daily intraperitoneal injections of 0, 0.1, 1 or 3 mg/kg MeHg chloride respectively from postnatal days (PD) 15-17, and then tested with the Morris water maze on PD45. After that the mice were sacrificed by cervical dislocation, and the protein levels of NMDA receptor subtypes in the hippocampus were measured by Western blot analysis. A significant increase in the latency (F=2.88, P<0.05) before finding the platform was observed in the 1 and 3 mg/kg MeHg exposure groups. Further, the 3 mg/kg MeHg exposure group also had a longer swim distance (F=2.97, P<0.05) for finding the platform. In the probe test, the MeHg exposure groups displayed a smaller number of platform crossings when the hidden platform was moved, but this did not reach statistical significance. Western blot analysis results showed significant increases in the levels of NR1, NR2A and NR2B proteins of the hippocampus in the 1 and 3 mg/kg MeHg exposure groups. Overall, the current study found that MeHg exposure at 1 and 3 mg/kg doses during the postnatal brain growth spurt induces subtle and persistent learning deficits, and the neurobehavioral abnormalities of MeHg-exposed mice might be ascribed to alteration of the gene expression of specific NMDA receptor subunits in the hippocampus.
Insights
Methylmercury (MeHg) exposure in mice during brain development caused learning deficits. This neurotoxicity may be linked to changes in NMDA receptor subunits in the hippocampus.
Area of Science:
- Neuroscience
- Toxicology
- Developmental Biology
Background:
- Methylmercury (MeHg) is a potent neurotoxin.
- Postnatal development is a critical period for brain growth and vulnerability to toxicants.
- NMDA receptors are crucial for learning and memory.
Purpose of the Study:
- To investigate the long-term effects of postnatal methylmercury exposure on learning and memory in mice.
- To examine the impact of methylmercury on NMDA receptor subunit expression in the hippocampus.
Main Methods:
- ICR mice received daily intraperitoneal injections of methylmercury chloride (0, 0.1, 1, or 3 mg/kg) from postnatal days 15-17.
- Morris water maze test was used to assess spatial learning and memory on postnatal day 45.
- Hippocampal protein levels of NMDA receptor subunits (NR1, NR2A, NR2B) were measured using Western blot analysis.
Main Results:
- Methylmercury exposure at 1 and 3 mg/kg significantly increased latency to find the platform in the Morris water maze.
- The 3 mg/kg group also showed a significantly longer swim distance.
- Western blot analysis revealed significant increases in hippocampal NR1, NR2A, and NR2B protein levels in the 1 and 3 mg/kg groups.
Conclusions:
- Postnatal methylmercury exposure at 1 and 3 mg/kg induces subtle but persistent learning deficits in mice.
- These neurobehavioral deficits may be associated with altered gene expression of specific NMDA receptor subunits in the hippocampus.
- The findings highlight the vulnerability of the developing brain to methylmercury toxicity.

