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ARTICLE
Mouse cerebellar Purkinje cell damage induced by diphenylhydantoin acute intoxication
Orlando J. CASTEJÓN*
Biological Research Institute and Faculty of Medicine, Zulia University, Maracaibo, Venezuela.
*Address correspondence to:Orlando J. Castejón,
BIOCELL 2015, 39(2-3), 33-40. https://doi.org/10.32604/biocell.2015.39.033
Abstract
Twenty one days old Swiss albino mice that received diphenylhydantoin (25 mg/kg, i.p., daily for
15 days) progressively developed gait alterations, changes of behavior and cerebellar ataxia. Cerebellar slices were
processed by conventional transmission electron microscopy. The body of Purkinje cells exhibited fragmented
limiting plasma membranes, dilated nuclear envelopes, swelling and disassembly of nuclear pores, enlargement
of rough and smooth endoplasmic reticulum and a notable detachment of membrane associated ribosomes, together with distorted vacuoles of smooth endoplasmic reticulum, bizarre shaped and swollen mitochondria with
dilated cristae, as well as disrupted limiting lysosomal membranes. Degenerated axosomatic synapses apparently
corresponding to basket cell axonal endings were recognized. Degenerated Purkinje cell axon initial segments
exhibited vacuolar degeneration of myelin sheath, dilated axoplasmic tubular bundles, fragmented axonal membranes, swollen mitochondria, and disassembly of cytoskeletal structures. Some edematous and clear secondary
and tertiary dendrites exhibited areas of dilated cisterns of smooth endoplasmic reticulum, clear and dark multivesicular bodies, and coated vesicles. Other dendritic ramifications exhibited an electron dense dendroplasm.
Degenerated and large climbing fiber endings were observed making axodendritic synapses with edematous
Purkinje dendrites. These presynaptic endings appeared depleted or containing few synaptic vesicles. These synapses did not exhibit pre- and postsynaptic densities. At the molecular layer, the edematous synaptic varicosities
of parallel fibers containing pleomorphic synaptic vesicles and dense extravesicular substance were observed
making asymmetric synaptic contacts with swollen Purkinje dendritic spines. These findings are postulated as
pathogenic mechanisms of mouse cerebellar ataxia.
Keywords
Cite This Article
CASTEJÓN, O. J. (2015). Mouse cerebellar Purkinje cell damage induced by diphenylhydantoin acute intoxication.
BIOCELL, 39(2-3), 33–40.
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