Posters
Presenting Author Academic/Professional Position
Padmanabhan Rengasamy
Academic Level (Author 1)
Faculty
Discipline/Specialty (Author 1)
Medical Education
Discipline Track
Biomedical Science
Abstract Type
Research/Clinical
Abstract
Background: Anencephaly, a severe form of congenital malformation of the brain and calvarium is reported to result from arrest of rostral neuropore closure. However, no clear mechanism has been discovered for anencephaly. Experimental models developed to study the mechanism have established a similar but less severe form of this anomaly called exencephaly. This phenotype is possibly due to the shorter gestational periods characteristic of experimental models of exencephaly. We had serendipitously discovered exencephaly when studying limb defects in rat embryos that were treated with cyclophosphamide on gestation day 12 after neural tube closure. We wished to determine whether exencephaly induced on gestation 12 would progress into anencephaly when gestation is prolonged.
Methods: We administered rats a single dose (15 mg/kg) of cyclophosphamide on day 12 of gestation and prolonged gestation by bilateral uterine ligation until post conception day 24. Controls were treated with saline.
Results: Fetal death was found to increase with prolongation of gestation. Living fetuses were growth restricted. Skeletal preparations revealed the consistent association of axial skeletal malformations in exencephaly fetuses. Histological preparations revealed extensive apoptosis, progressive hydrocephaly and increased intraventricular pressure that intensified with advancing gestation. Proliferation of choroid plexus was extensive. Ependyma was denuded and neural mass lay free in ventricles. The capillary network around the brain tissue was highly proliferative and penetrated the disintegrating brain. Hemorrhage, edema and parenchymal tissue loss seemed to progress unabated. Cystic spaces appeared beneath the base of the brain and appeared like pushing neural tissue out of the shallow cranial fossae. By post-conception day 24, most of the brain tissue had degenerated.
Conclusion: The results provide clear evidence of secondary reopening of closed neural tube in the pathogenesis of anencephaly in this model.
Presentation Type
Poster
Recommended Citation
Rengasamy, Padmanabhan, "Developmental bases of open neural tube defects in rat embryos" (2025). Research Colloquium. 54.
https://scholarworks.utrgv.edu/colloquium/2022/posters/54
Included in
Developmental bases of open neural tube defects in rat embryos
Background: Anencephaly, a severe form of congenital malformation of the brain and calvarium is reported to result from arrest of rostral neuropore closure. However, no clear mechanism has been discovered for anencephaly. Experimental models developed to study the mechanism have established a similar but less severe form of this anomaly called exencephaly. This phenotype is possibly due to the shorter gestational periods characteristic of experimental models of exencephaly. We had serendipitously discovered exencephaly when studying limb defects in rat embryos that were treated with cyclophosphamide on gestation day 12 after neural tube closure. We wished to determine whether exencephaly induced on gestation 12 would progress into anencephaly when gestation is prolonged.
Methods: We administered rats a single dose (15 mg/kg) of cyclophosphamide on day 12 of gestation and prolonged gestation by bilateral uterine ligation until post conception day 24. Controls were treated with saline.
Results: Fetal death was found to increase with prolongation of gestation. Living fetuses were growth restricted. Skeletal preparations revealed the consistent association of axial skeletal malformations in exencephaly fetuses. Histological preparations revealed extensive apoptosis, progressive hydrocephaly and increased intraventricular pressure that intensified with advancing gestation. Proliferation of choroid plexus was extensive. Ependyma was denuded and neural mass lay free in ventricles. The capillary network around the brain tissue was highly proliferative and penetrated the disintegrating brain. Hemorrhage, edema and parenchymal tissue loss seemed to progress unabated. Cystic spaces appeared beneath the base of the brain and appeared like pushing neural tissue out of the shallow cranial fossae. By post-conception day 24, most of the brain tissue had degenerated.
Conclusion: The results provide clear evidence of secondary reopening of closed neural tube in the pathogenesis of anencephaly in this model.
