Abstract
The choroid plexus in the N-methylnitrosourea (MNU)-induced dysgenetic hydromicrocephalic rat offsprings was examined morphologically at the ages of 1, 3, 12, and 27 weeks. Hydromicrocephalus became more severe with advanced age, and apparent desquamation of choroidal cells and interstitial edema were first detected at the age of 12 weeks. At the age of 27 weeks, a decrease in number and size of choroidal cells and remarkable edematous widening of the interstitium were noticed. Ultrastructually, at the age of 3 weeks, the choroidal cells with decreased or irregularly distributed nuclear chromatin and narrower cisternae of rough endoplasmic reticulum were prominent. At the luminal surface of these cells, microvilli were anomalous in number and size, and intercellular spaces were slightly dilated. In the interstitium there were distention of perivascular spaces and increase in number of pinocytotic vesicles in the capillary endothelium. At the age of 12 weeks degenerated choroidal cells showed irregular distribution of nuclear chromatin and had a large number of rough endoplasmic reticulum showing short tubular structures. Microvilli were severely destructed into membraneous and fused forms. Membraneous or floccurent materials were present in markedly dilated Golgi saccules and intercellular spaces. In the interstitium, prominent dilatation of perivascular spaces and flattened capillary endothelial cells were observed. These findings suggest that excessive leakage of blood plasma through the choroidal epithelium into the lumen and reduction of reabsorptive function of choroidal cells are important for the cause of the hydrocephalus.
