Biomedical Sciences ETDs

Publication Date

Fall 12-12-2020

Abstract

Background: Depression and anxiety disorders, believed to be caused by stress-related neuropeptides and pro-inflammatory molecules in the brain, are prevalent comorbidities of fetal alcohol spectrum disorders (FASD).

Methods: Brain tissue was collected following a 4-hour maternal separation stress during the early postnatal period, postnatal days 10 and 12, from mice subjected to 1st and 2nd trimester prenatal alcohol exposure (PAE).

Hypothesis: We hypothesized that PAE leads to glucocorticoid receptor insensitivity, stress molecule overexpression, and potentiated toll-like receptor 4 (TLR4) pathway inflammatory responses in the brain following early life stress.

Results: PAE and stress increased mRNA expression of TLR4 activation markers, stress-associated neuropeptides, and glucocorticoid receptor regulators in the amygdala in females only while changes were blunted in the hypothalamus.

Conclusion: Exacerbated reactions to early postnatal stress in PAE offspring may alter the developmental trajectory of the brain stress system, underlying increased incidence of anxiety and depression in FASD adults.

Keywords

Prenatal alcohol exposure, Early life stress, Toll-like receptor 4, Depression, Anxiety

Document Type

Thesis

Language

English

Degree Name

Biomedical Sciences

Level of Degree

Masters

Department Name

Biomedical Sciences Graduate Program

First Committee Member (Chair)

Dr. Erin Milligan

Second Committee Member

Dr. Shahani Noor

Third Committee Member

Dr. C. Fernando Valenzuela

Fourth Committee Member

Dr. Nora Perrone-Bizzozero

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