Submission Date

7-19-2019

Document Type

Paper- Restricted to Campus Access

Department

Neuroscience

Second Department

Biology

Faculty Mentor

Carlita Favero

Student Contributor

Paige Springmann

Comments

Presented during the 21st Annual Summer Fellows Symposium, July 19, 2019 at Ursinus College.

Project Description

Fetal alcohol spectrum disorder (FASD) refers to several conditions all caused by prenatal alcohol exposure (PAE). PAE may cause difficulties with sensory processing. These difficulties suggest thalamocortical axons (TCAs), which carry sensory information to cortical processing areas, may be impacted by PAE. TCAs fail to reach the cortex in cases of PAE, indicating that PAE may target TCA migration. TCAs are guided during their migration from the thalamus to the cortex partly by different types of cells, including a cell population called corridor cells. Corridor cells guide TCAs through the medial ganglionic eminence (MGE), a region of the developing brain which is otherwise non-permissive to TCAs. We hypothesize that PAE widens the corridor region of the MGE, which would prevent corridor cells from properly guiding TCAs. We are developing an in situ hybridization protocol using digoxigenin-labeled Ebf1 riboprobes to visualize corridor cells and determine whether corridor cell distribution is impacted by PAE. To model PAE, we injected pregnant Swiss Webster dams with 20% ethanol from embryonic days (E) 7.5 to 13.5. On E13.5, embryos were removed via C-section, embedded in paraffin, and sectioned at 5 microns in the sagittal orientation. In the future, we hope to expand this protocol to coronal sections. Following in situ hybridization, we will measure the dimensions of the corridor to quantify effects of PAE. We will also analyze sex differences in corridor width. A wider corridor in alcohol-exposed embryos may alter TCA migration, potentially leading to sensory deficits in FASD.

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