Axonal damage associated with enlargement of ventricles during hydrocephalus: A silver impregnation study

Citation
Yh. Ding et al., Axonal damage associated with enlargement of ventricles during hydrocephalus: A silver impregnation study, NEUROL RES, 23(6), 2001, pp. 581-587
Citations number
50
Categorie Soggetti
Neurosciences & Behavoir
Journal title
NEUROLOGICAL RESEARCH
ISSN journal
01616412 → ACNP
Volume
23
Issue
6
Year of publication
2001
Pages
581 - 587
Database
ISI
SICI code
0161-6412(200109)23:6<581:ADAWEO>2.0.ZU;2-4
Abstract
Motor and cognitive deficits are commonly associated with hydrocephalus. Al though the mechanisms responsible for these impairments have not been confi rmed, neuronal cell death and axon degeneration may play an important role, and have long lasting consequences on neuronal connectivity. The goal of t his study was to determine if neural degeneration occurred during hydroceph alus in structures anatomically related to cognitive motor functioning, nam ely, the sensorimotor cortex, neostriatum, hippocampus and corpus callosum. Neural damage, as visualized by silver staining, was examined in adult rat s 2-10 weeks after obstructive hydrocephalus was induced by kaolin injectio n into the cisterna magna. In mild or moderate hydrocephalus, mostly occurr ing 2-6 weeks after kaolin injections, silver-labeled axons were scattered in the white matter of the sensorimotor cortex, corpus callosum, neostriatu m, and hippocampus. in severe hydrocephalus, 10 weeks after kaolin injectio ns, axon degeneration was more extensive in these areas, as well as in laye rs IV through VI of the sensorimotor cortex. Axons in the subiculum and the fimbria were heavily labeled, suggesting damage to hippocampal afferent an d efferent fibers. In contrast, neuron cell death was rarely observed at an y stage of hydrocephalus. The major pathological change of brain regions in volved in motor and learning functions during hydrocephalus is axon degener ation, and this degeneration is correlated with an enlargement of the cereb ral ventricles.