Exposure to trimethyltin significantly enhances acetylcholinesterase staining in the rat dentate gyrus.
Trimethyltin (TMT) is known to produce substantial damage to the hippocampal formation. It also destroys neurons within the entorhinal cortex, thereby causing degeneration of perforant path afferents that terminate in the outer molecular layer (OML) of the dentate gyrus. Surgical destruction of the entorhinal cortex also causes the perforant path to degenerate. This leads to reactive synaptogenesis (axonal sprouting) of septal afferents to the dentate gyrus. The purpose of the present study was to determine whether administration of 6 mg/kg of TMT by gavage to rats would cause axonal sprouting within the septo-dentate projection. A histochemical stain for acetylcholinesterase (AChE) was used. Compared to control subjects rats given TMT exhibited significantly denser AChE staining in the dentate OML. This is putative indication of reactive synaptogenesis within the cholinergic projection to this layer of the dentate and is somewhat surprising because other neurotoxins, such as lead and ethanol, that affect neurons within the hippocampal formation reduce the capacity for reactive synaptogenesis in response to lesions of the entorhinal cortex.
Department of Anatomy, Quillen-Dishner College of Medicine, East Tennessee State University, Johnson City 37614.
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Woodruff
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Baisden
D000110:Acetylcholinesterase / Q000096:biosynthesis*; D000818:Animals; D006624:Hippocampus / Q000187:drug effects* / Q000201:enzymology; D008297:Male; D051381:Rats; D013194:Staining and Labeling; D014220:Trialkyltin Compounds / Q000633:toxicity*; D014298:Trimethyltin Compounds / Q000633:toxicity*
D014220:Trialkyltin Compounds; D014298:Trimethyltin Compounds; C040533:trimethyltin chloride; D000110:Acetylcholinesterase