TRIETHYLTIN TOXICITY AS A MODEL FOR DEGENERATIVE DISORDERS

Triethyltin (TET) toxicity in mice was examined as a model for certain degenerative disorders. Spontaneous and elicited behavioral tests, electrophysiological measures and nervous system protein characterizations were used to study anomalies resulting from TET treatments. TET animals exhibited lowered spontaneous locomotor activity levels, increased sciatic nerve excitation threshold and conduction velocities and increased power levels in the slower frequency components of their EEG. Performances in an active avoidance task and nervous system protein compositions were not altered as a consequence of TET treatments. The gross ultrastructural changes commonly seen in TET intoxication may not primarily responsible for the observed neurophysiological changes. Possible sites of action of TET, in both the peripheral and CNS that would produce these neurophysiological changes and the relationship of these changes to the behavioral symptoms were discussed.