ABSTRACT
Hydrocephalus is an accumulation of cerebrospinal fluid (CSF) with dilatation of brain ventricles which can be either communicating or non-communicating. Multiple pathophysiological mechanisms underlie the appearance of hydrocephalus, which has many different causes including birth defects, brain hemorrhage, infection, meningitis, tumor, or head injury. The choroid plexuses (ChP) are circumventricular structures closely related to the above-mentioned pathophysiological mechanisms of the CSF, and aquaporin-1 (AQP1) is the water channel directly implicated in CSF production. Our studies with hydrocephalic rats revealed an increase and redistribution of AQP1 in the ChP, with AQP1 being expressed not only in the cell apical pole, but also in the cell basal pole and in the stroma. The immunohistochemical changes observed in both communicating and non-communicating hydrocephalus suggest a variation in the efficiency of the cells of the ChP, where AQP1 could perform both CSF production and reabsorption in order to delay ventricular dilatation
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