Abstract
Children with Fetal Alcohol Spectrum Disorder (FASD) have impaired sensory processing skills as a result of neurodevelopmental anomalies. The somatosensory barrel field of rodent brain is a readily accessible model for studying the effects of alcohol exposure. Within the barrel field, the posterior medial barrel subfield (PMBSF) receives sensory inputs from the large vibrissae on the contralateral face. This study reports on the consequence of prenatal exposure to alcohol on the somatosensory cortices of mice later in life. Two control groups, a sucrose and a non-treated control, were also examined. At postnatal day (PND) 56 the cerebral hemisphere of mice from each group were processed for cytochrome oxidase reactivity. In contrast to previous studies, there were no significant differences in the mean areas of: (I) the PMBSF enclosure, (II) the PMBSF barrels, (III) the individual PMBSF barrels and (IV) the septal portion of the PMBSF in the alcohol group compared to the controls. However barrel sizes in rows D and E in the alcohol group were significantly reduced, indicating an alcohol-induced damage on the barrel development and which may reduce the amount of the cortex devoted to processing somatosensory input– a common defect seen in children with FASD.
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