Effects of prenatal alcohol exposure on the development of the somatosensory cortical barrels in C57BL/6 mice
Prior work has shown that the serotonin (5-HT) system is negatively affected by prenatal alcohol exposure (PAE). The development of the sensory cortical barrels is dependent on 5-HT input and 5-HT-rich thalamocortical afferents. Therefore, it is hypothesized that prenatal exposure to alcohol will deleteriously affect the normal development of the cortical barrel network. The results of this dissertation demonstrated a nearly 50% reduction in NeuN-positive neuronal nuclei within the barrel patches of rows B and C of the PMBSF in all barrels sampled when counted with stereology as well as a reduction in barrel volume in barrel arcs 1 and 2. In addition, prenatal alcohol exposure reduced the total posterior medial barrel subfield (PMBSF) area, as well as the areas of the individual barrels within the PMBSF, observed using both 5-HT and cytochrome oxidase staining relative to chow but not pair-fed controls There were no group differences in the number of immature neurons labeled using an antibody to Hu C/D, an mRNA binding protein expressed in mature neurons. Finally, treatment with buspirone, a 5-HT1A agonist, concurrent with liquid diet consumption, was able to prevent the alcohol-induced deficits seen in total NeuN-positive neuron number following PAE, but did not protect against effects on the area or volume measurements of the PMBSF. The dramatic reduction in neurons within these sensory barrels following PAE and the reduction in the size of the PMBSF may underlie a change in the discriminatory sensitivity of the whiskers. These data support the hypothesis that the PAE-induced reductions in neuron number are related to developmental abnormalities in serotonin since buspirone, a 5-HT1A agonist known to prevent 5-HT developmental deficits, was able to prevent these cortical neuronal deficits. Supported by NIH AA12406, AA07462.
Goodlett, Purdue University.
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