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Trimethyltin-induced alterations in behavior are linked to changes in PSA-NCAM expression
A K Halladay1, D T Wilson, G C Wagner
1Joint Graduate Program in Toxicology, Rutgers University, Piscataway, NJ, USA.
Neurotoxicology
|January 24, 2006
Summary
Trimethyltin (TMT) exposure impairs spatial learning and reduces polysialylated neural cell adhesion molecule (PSA-NCAM) in mice. However, these effects are transient, with recovery observed after 168 hours.
Area of Science:
- Neuroscience
- Neurotoxicology
- Molecular Biology
Background:
- Trimethyltin (TMT) is a neurotoxin damaging the hippocampus and limbic system.
- TMT exposure decreases polysialylated neural cell adhesion molecule (PSA-NCAM) in the mouse hippocampus.
- PSA-NCAM is crucial for neural plasticity and memory formation.
Purpose of the Study:
- To investigate the association between spatial learning deficits after TMT exposure and changes in NCAM-180 and PSA-NCAM levels.
- To determine the impact of TMT exposure at different learning stages on spatial memory and PSA-NCAM expression.
Main Methods:
- Mice were treated with TMT or saline before or after spatial learning training (water maze).
- Spatial learning, motor activity, and light avoidance were assessed at various time points post-treatment.
- Hippocampal and frontal cortex levels of NCAM and PSA-NCAM were analyzed.
Main Results:
- TMT exposure impaired spatial learning and blocked learning-induced PSA-NCAM elevations for 24-96 hours, with recovery by 168 hours.
- Spatial learning improvements correlated with elevated hippocampal PSA-NCAM.
- TMT exposure during learning reconsolidation caused transient deficits but did not attenuate PSA-NCAM.
Conclusions:
- PSA-NCAM plays a specific role in the acquisition and consolidation of spatial memory.
- TMT-induced spatial learning deficits are linked to altered PSA-NCAM expression.
- The timing of TMT exposure influences its impact on spatial memory and PSA-NCAM levels.
