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mutant mice suffer a congenital hydrocephalus trig-gered by ependyma denudation [1]. The ventricular sur-face in non hydrocephalic newborn mice is lined by theimmature ependyma, which is characterized for beingvimentin (-) and S100β (-), at variance in the adult ani-mals the mature ependyma expresses vimentin and S100 β[2]. On the other hand, in the hydrocephalic mice theependyma begins to denudate on the 12th day of gesta-tion, and at PN8 only some areas of lateral ventricle arestill endowed with ependyma. In parallel, astroglia startsto cover the denuded surface forming a new cell layer, theglial scar, which lines the damaged ventricular surface. Wehave studied the permeability to horseradish peroxidase(HRP) of these four regions at the ventricular wills:mature ependyma, and denuded areas with or withoutglial scar.

cerebrospinal fluid research

Differential permeability to horseradish peroxidase in affected and non-affected ventricular walls during postnatal development of normal and hydrocephalic hyh mice