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

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Author(s): Prakash | Singh G | Singh S

Journal: Neuroanatomy
ISSN 1303-1783

Volume: 6;
Issue: 1;
Start page: 1;
Date: 2007;
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Keywords: apoptosis | cerebral aqueduct | cerebro spinal fluid | cyclophosphamide | ependymal cells | hydrocephalus

ABSTRACT
This study aims to understand the mechanism of failure of canalization of cerebral aqueduct following intrauterine exposure to reference teratogen, cyclophosphamide in murine pups. Non-canalization of cerebral aqueduct was found to result in internal hydrocephalus. Cyclophosphamide was administered to pregnant mice on day 10, 11, or 12 of gestation in a single dose of 20 mg/kg body weight. Fetuses were dissected out on day 19 and studied for hydrocephalus and other cerebral or cranial malformations. Serial sections of brain in coronal and transverse planes exhibited incomplete development and failure of canalization of cerebral aqueduct.Pressure of cerebrospinal fluid (CSF) in non-canalized aqueduct resulted in its rupture leading to leakage andaccumulation of CSF in brain substance causing a cavity full of CSF close to unopened aqueduct. The large poolof CSF in the brain substance in extreme cases communicated with the subarachnoid space pushing through thesubstance of brain causing external hydrocephalus. Internal hydrocephalus on the other hand was resulted fromback pressure of CSF following blockage in its flow due to non-canalization of the cerebral aqueduct. In theextreme cases internal and external hydrocephalus were seen intercommunicating. Cyclophosphamide inducedinhibition of mitosis and cell differentiation of ependymal cells and augmentation of apoptosis of brain cellswere attributed as the major causes underlying the incomplete development of cerebral aqueduct. The studyalso suggested inductive role of CSF in the differentiation of ependymal cells lining the cerebral aqueduct.
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