Date of Award

Summer 5-30-2024

Document Type

Thesis (Master's)

Department or Program

Biochemistry and Cell Biology

First Advisor

Hermes Yeh

Abstract

Atypical tactile responses are implicated in Fetal Alcohol Spectrum Disorders (FASD). Our lab reported diminished tactile sensitivity in young adolescent mice with a history of prenatal alcohol exposure (PAE). Here, I employed immunohistochemistry to investigate the anatomical correlates of altered tactile sensitivity observed in mice with PAE. Using our 3-day binge paradigm, I examined changes in the distribution pattern of pre- (thalamocortical afferents) and postsynaptic (pyramidal neurons) partners involved in processing tactile information in the SSC of Postnatal day (P) 7 mice. In rodents, tactile information is relayed somatotopically to the SSC via TC afferents expressing vesicular glutamate transporter 2 (vGlut2) and aggregating in 'barrels' in L4, in addition to innervating other layers. With PAE, there was a significant decrease in vGlut2 immunofluorescence intensity in L4 SSC. Moreover, we found the average barrel width to be significantly larger with PAE, indicating disrupted barrel development, consistent with previous studies employing different PAE paradigms. Moreover, ethanol exposure resulted in a significant increase in two main subpopulations of pyramidal neurons: Special AT-rich sequence-binding protein 2 (Satb2)-expressing callosal (CPN) and COUP TF1-interacting protein 2 (Ctip2)-expressing subcortical projection neurons (SCPN) in the SSC. These immunohistochemistry-based findings suggest PAE-induced anatomical changes in SSC.

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