Mouse Cerebellar Ataxia Following Acute Diphenylhydantoin Intoxication. III. Stellate Neuron Morphopathological Changes Induced by Diphenylhydantoin (DPH)
Mouse cerebellar stellate neurons with diphenylhydantoin-induced cytotoxic edema were examined with the transmission electron microscope to study the submicroscopic pathology of neuronal bodies and their synaptic connections in order to obtain a better insight of morphopathogenetic mechanisms of mouse cerebellar ataxia. Thirty 21 days postnatal Swiss albino mice received intraperitoneal injection of 5.5 diphenylhydantoin (Dilantin) at 35 mg/kg daily for 15 days developing progressively gait alterations, changes of behavior and cerebellar ataxia. A control group of thirty normal and healthy Swiss albino mice were used as controls. Stellate neuronal cytoplasm exhibited endoplasmic reticulum stress featured by enlargement of endoplasmic reticulum cisterns and detachment of associated ribosomes, edematous mitochondria, vacuolization, and necrotic areas of limiting plasma membrane. The Golgi apparatus showed edematous changes, fragmentation and increased amount of Golgi and complex vesicles. Lysosomes displayed vacuolization and limiting plasma membrane fragmentation. Microtubular disassembly also was observed. The degenerated axomatic and axodendritic junctions of incoming parallel and climbing fibers, basket cell and other stellate axonal endings showed enlargement of synaptic vesicles, preservation and/or absent preand postsynaptic densities. Edematous serotoninergic afferent fiber endings upon stellate neuronal soma contained a mixed population of clear and dense-cored synaptic vesicles and absence of pre- and postsynaptic endings. The findings are related with morphopathogenetic mechanisms of cerebellar ataxia and mouse changes of behavior.
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Document Type: Research Article
Publication date: June 1, 2016
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