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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.

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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.