Quality and quantitative morphological changes in the brain of adult mice used as an animal model of fetal alcohol syndrome

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dc.contributor.author Olateju, Oladiran Ibukunolu
dc.date.accessioned 2018-02-21T07:56:01Z
dc.date.available 2018-02-21T07:56:01Z
dc.date.issued 2017
dc.identifier.uri https://hdl.handle.net/10539/24051
dc.description A Thesis submitted to the Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, in fulfilment of the requirements for the degree of Doctor of Philosophy Johannesburg, 2017 en_ZA
dc.description.abstract We examined the effect of chronic prenatal alcohol exposure on the qualitative and quantitative changes in the brain of C57BL/6J mice once they had reached early adulthood (56 days post-natal). Pregnant mice, and their in utero litters, were exposed to alcohol, through oral gavage, on gestational days 7 – 16, with recorded blood alcohol concentrations averaging 1.84 mg/ml (chronic alcohol, or CA, group). Two control groups, an oral gavage sucrose control group (chronic alcohol control, or CAc, group) and a non-treated control group (NTc group), were also examined. Using appropriate antibodies specific for the neurons or nuclei of interest, the present study compared morphologically and quantified (I) the neuronal cell proliferation and the appearance of immature neurons in the hippocampal adult neurogenesis, (II) the changes in the PMBSF barrel sizes in the somatosensory cortex, (III) the cortical organization, cell number and cell sizes of cerebellar interneurons in the vermal cerebellum, and (IV) the nuclear organization, cell number and cell sizes of four specific clusters of nuclei for the control and regulation of sleep-wake cycle in the brains of all the experimental groups. The stained neurons and nuclei of interest were consistent in all the three experimental groups. The quantitative analyses showed that alcohol, in comparison with the two controls, had (I) no strong effect on the proliferative process but significantly reduced the numbers of immature neurons in the hippocampus, (II) no effect on the barrel sizes from the different measured parameters, despite a reduced barrel size in the alcohol group, but there was significant size reductions in barrel rows D and E, (III) no effect on the cell densities of Nissl and PV+ stained neurons in the molecular layer and the cell sizes of Purkinje cells immunolabelled with CB antibody, and (IV) no effect on the numbers of ChAT+ neurons, TH+ neurons, OxA+ neurons, however there were significantly larger OxA+ neurons and significantly smaller ChAT+ neurons while the TH+ neuron size was not significantly different. Some of these results are consistent with other studies that utilized FAS rodent models thus suggesting the suitability of this mouse model for FAS studies. The significant findings could help explain the reasons for the neurodevelopmental and behavioural problems that are common to FAS subjects. The neuroanatomical evidence presented in this study could open avenues for interventions to improve the quality of life of FAS and FASD children. en_ZA
dc.language.iso en en_ZA
dc.subject.mesh Fetal Alcohol Spectrum Disorders
dc.title Quality and quantitative morphological changes in the brain of adult mice used as an animal model of fetal alcohol syndrome en_ZA
dc.type Thesis en_ZA
dc.description.librarian MT 2018 en_ZA

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