Abstract :
Timed pregnant wistar rats were divided randomly into groups A and B (n=6) each and C (n=4). Group A received a daily ethanol dose of 5.8 g/kg body weight per day, at 16.00 h on days 9–12th of gestation by intragastric intubations. Group B was pair-fed along with the treated rats and received an isocaloric solution of sucrose to substitute for the ethanol in the experimental group, for the same duration, while group C received standard chow and water ad libitum. The adult offsprings at 42 days of age, (n=10) from each group were sacrificed by whole body perfusion-fixation, after anaesthesia by an overdose of penthotal intraperitoneally. Specimens of neocortical samples were processed routinely for paraffin embedding and sections of 6 μm thickness stained for neurohistology. Another set of specimens was cryosectioned at −23 °C after cryoprotection in 30% sucrose/PBS and evaluated for GFAP immunohistochemistry. The study showed a distortion of the microanatomy of the neocortex in the treatment group A, particularly of layer V pyramidal neurons, which revealed mostly pyknotic pyramidal neurons with broken dendrites, collapsed cell bodies, obliterated nuclei and nucleoli. No differences were found between the brains from rats in groups B and C. There were widespread focal areas of reactive astrogliosis, more prominent within the layer V. Astrocytes demonstrated highly stained GFAP-positive immunoreactivity with heavy fibrillary processes in the neocortex of group A offsprings compared to the controls. The sub-pial regions were, however, sparse. In conclusion, this study confirms the hypothesis that microanatomical and microchemical changes following prenatal ethanol exposure persist into adulthood in rats.
Keywords :
Cerebral cortex , Pia mater , fetal alcohol syndrome , Adult rats , Astrocytes , Birth defects , Astrogliosis