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 electroencephalograms. Performance in an active avoidance task suggest that the gross ultrastructural changes commonly seen in TET intoxication are not primarily responsible for the observed neurophysiological changes. Possible sites of action of TET, in both the peripheral and central nervous systems, that would produce these neurophysiological changes and the relationship of these changes to the behavioral symptoms are discussed.
D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D003711:Demyelinating Diseases / Q000503:physiopathology*; D004195:Disease Models, Animal; D004569:Electroencephalography; D005071:Evoked Potentials / Q000187:drug effects; D005260:Female; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D009419:Nerve Tissue Proteins / Q000378:metabolism; D010525:Peripheral Nerves / Q000187:drug effects; D012584:Sciatic Nerve / Q000378:metabolism; D013997:Time Factors; D014220:Trialkyltin Compounds / Q000633:toxicity*; D014267:Triethyltin Compounds / Q000494:pharmacology / Q000633:toxicity*
D009419:Nerve Tissue Proteins; D014220:Trialkyltin Compounds; D014267:Triethyltin Compounds