Mouse Cerebellar Ataxia Following Acute Diphenylhydantoin Intoxication. IV. Bergmann Glial Cell Pathology Induced by Diphenylhydantoin (DPH) in Mouse Cerebellar Cortex
In the present paper we describe the reactivity and hypertrophic changes of diphenylhydantoin (DPH)-induced changes in mouse cerebellar Bergmann glial cells. Twenty one days postnatal swiss albino mice received intraperitoneal injection of 5.5 diphenylhydantoin (DPH) at 25 mg/kg daily for 15 days developing progressively gait alterations, changes of behavior and cerebellar ataxia. Cerebellar slices were processed by conventional transmission electron microscopy. Bergmann glial cell showed swollen and hypertrophic cytoplasm containing dark and swollen mitochondria, vacuolated lysosomes, fragmented Golgi apparatus and small, medium and large vacuoles. Fragmented microtubules and large lipofuscin granules also were found. The Bergmann gial fibers also exhibited edematous and hypertrophic changes, vacuolated phagosomes, degenerated mitochondria, and vacuoles. Swollen glial cytoplasm was observed at the medium and outer third cerebellar molecular layer surrounding clear and dense Purkinje dendrites, the bundles of parallel fibers and their synaptic varicosities, and parallel fibers-Purkinje dendritic spines. These latter exhibit degenerated features characterized by enlargement of synaptic vesicles. The Purkinje-Bergmann glia unit is disrupted by DPH intoxication. We suggest a role of swollen and hypertrophic Bergmann glial cells in the pathogenesis of mouse cerebellar ataxia.
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Document Type: Research Article
Publication date: 01 December 2016
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