Submission Date

7-21-2016

Document Type

Paper- Restricted to Campus Access

Department

Biology

Second Department

Neuroscience

Faculty Mentor

Carlita Favero

Comments

Presented during the 18th Annual Summer Fellows Symposium, July 22, 2016 at Ursinus College.

Supported by a Howard Hughes Medical Institute (HHMI) grant.

Project Description

Fetal Alcohol Spectrum Disorders (FASD) is an umbrella term describing developmental abnormalities in sensation, perception, learning, and behavior caused by ethanol exposure during pregnancy. Alcohol exposure causes alterations in sensation and perception abilities. These could be compromised due to developmental deformities of forebrain axon tracts, including the thalamocortical axon (TCA) tract. This tract connects the thalamus and cortex, sending sensory information through the brain. Exploring processes of FASD could reveal that TCAs are altered due to defects in guidance mechanisms, which lead axons to their final destination in the cortex. Following an alcohol exposure during development, we believe the Slit/Robo pathway could be altered. This pathway is an important guidance mechanism to guide TCAs through the medial ganglionic eminence (MGE) and lateral ganglionic eminence (LGE) into the cortex. To investigate this hypothesis, we utilize a drinking in the dark paradigm in Swiss Webster mice to model voluntary drinking (Boehm, 2008). The mice are given either a saccharin or a saccharin-sweetened ethanol solution for two hours daily. To visualize gene expression, we used in situ hybridization. The first attempt was to visualize Ebf1 expression, a previously successful method in our lab. Ebf1 is a LGE marker, used to locate a region along the TCA pathway called the corridor. The focus was shifted to Robo1 to investigate if expression levels were decreased. It is the hope that with developing a more stringent protocol, in situ hybridization staining will be successful in future research, with the goal of comparing ethanol-exposed and control brains.

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