Effects of prenatal alcohol exposure on the development of the vibrissal somatosensory cortical barrel network.

We have previously shown that the serotonin (5-HT) and its thalamocortical afferents are compromised by prenatal alcohol exposure (PAE). The development of the sensory cortical barrels is regulated by 5-HT-rich thalamocortical afferents. Therefore, it is hypothesized that PAE will deleteriously affect the postnatal development of the cortical barrel formations. On embryonic day (E)7, C57BL/6 mice were grouped into: Alcohol (Alc), Pair-fed (PF), or Chow, and maintained on diet until E18. On postnatal day 7, cortices were stained with 5-HT for thalamocortical fibers, and a NeuN for identification of mature neurons. The area of the posterior medial barrel subfield (PMBSF), was measured as well as the number of NeuN+ neurons within the barrel patches. Though brain weight and brain volume were similar among the three groups, a significant reduction was seen in total area of the PMBSF, and in the average individual barrel area in the Alc group as compared to Chow. Furthermore, the volumes of the B, but not C row barrels were significantly reduced. Barrels were found missing in layer IV, specifically in the posterior aspects of the A, B, and straddler row in the Alc group. Cell counts demonstrated a nearly 50% reduction in NeuN+ neuron number in both rows. This reduction in size of the PMBSF and fewer neurons within these sensory barreloids may underlie a change in the development of the discriminatory sensitivity of the whiskers and serves as an excellent model for the study of a compromised sensory modality following PAE.