Ependyma: normal and pathological. A review of the literature.
A review of the available literature reveals that proliferation of ependyma occurs during embryological and early postnatal periods of development. Turnover, however, declines significantly during postnatal life and only low levels of residual activity persist into adulthood under normal conditions. In some regions of the ventricle, however, morphological and histochemical differentiation of ependyma is not attained for some considerable time postnatally. Recent immunocytochemical studies using GFAP indicate that only tanycytes may acquire antigenicity during development and that they may share a common phylogeny and/or function with astrocytes. Under pathological conditions, the bulk of available evidence suggests that inherent differences may exist in the proliferative capacity of ependyma in different regions of the neuraxis. Although the response of ependyma to various pathological conditions is equivocal, proliferation has been often observed in response to spinal cord injury. Indeed, ependyma is believed to play a significant role in the initiation and maintenance of the regenerative processes in the spinal cord of inframammalian vertebrates. In hydrocephalus there appears to be a remarkable similarity in cytopathological changes regardless of the mode of induction. The sequence, severity and extensiveness of damage appear to correlate with the degree of ventricular dilatation. The most commonly observed changes are (1) stretching and flattening of ependyma, most pronounced over white matter, (2) characteristic ependymal cell surface changes associated with ventricular distension, (3) increased extracellular space and periventricular edema and (4) demyelination and subependymal gliosis. Although ependymal cell proliferation has been reported as part of the overall tissue response to chronic hydrocephalus and to the pathology of ventricular shunt occlusion, the evidence is not entirely convincing and there is clearly a need for further research on the subject.
D000818:Animals; D002454:Cell Differentiation; D002455:Cell Division; D004805:Ependyma / Q000254:growth & development / Q000473:pathology* / Q000502:physiology; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006801:Humans; D006849:Hydrocephalus / Q000151:congenital / Q000209:etiology / Q000473:pathology*; D006867:Hydrolases / Q000378:metabolism; D051379:Mice; D008995:Monoamine Oxidase / Q000378:metabolism; D010088:Oxidoreductases / Q000378:metabolism; D010903:Pituitary Gland, Anterior / Q000502:physiology; D051381:Rats; D013119:Spinal Cord Injuries / Q000473:pathology; D013723:Teratogens; D014777:Virus Diseases / Q000150:complications; D014945:Wound Healing
D005904:Glial Fibrillary Acidic Protein; D013723:Teratogens; D010088:Oxidoreductases; D008995:Monoamine Oxidase; D006867:Hydrolases