Cyclophosphamide induced non - canalization of cerebral aqueduct resulting in hydrocephalus in mice

Cyclophosphamide, a model teratogen, has been used to produce hydrocephalus experimentally by various researchers [1–4]. Although the precise mechanism of cyclophosphamide induced hydrocephalus remains elusive, hypertrophy of choroid plexus was considered as the primary cause [1,4]. Singh et al [4] observed agenesis or stenosis of the aqueduct as an associated reason. The present work has been undertaken to elucidate the mechanism involved in cyclophosphamide induced hydrocephalus in mice. The present study reports a novel observation that intrauterine exposure of fetuses to cyclophosphamide leads to an incomplete canalization of cerebral aqueduct resulting in both internal and external hydrocephalus; i.e., CSF accumulation in both ventricles of brain and subarachnoid space. The report further discusses cyclophosphamide induced interference in cell differentiation and mitosis in ependymal cells as the possible mechanism of incomplete canalization of cerebral aqueduct. Furthermore, it provides evidence to show that CSF plays a pivotal role in the differentiation of ependymal cells lining the cerebral aqueduct.