Submission Date

7-24-2020

Document Type

Paper- Restricted to Campus Access

Department

Neuroscience

Faculty Mentor

Carlita Favero

Comments

Presented during the 22nd Annual Summer Fellows Symposium, July 24, 2020 at Ursinus College.

A related presentation is available here.

Project Description

Fetal Alcohol Spectrum Disorder (FASD) describes the range of deficits that arise from prenatal alcohol exposure. When a pregnant mother drinks alcohol, these deficits can present in offspring as physiological abnormalities, cognitive and sensory defects, or a combination. One particular brain region in which we see consistent deficits in FASD is the corpus callosum (CC), the major white matter tract which connects the two brain hemispheres. CC development is very specific, so a problem in any one of the mechanisms involved can lead to significant abnormalities. The CC is formed by callosal axons which are guided toward and across the midline by pioneer axons, guidance cues, as well as other neuronal and glial populations before projecting into the opposite cortex. In studies where some of these mechanisms were absent, such as in Netrin-1/DCC(a guidance cue/receptor family) mutants, the CC was completely or partially absent. These findings emphasize the importance of these guidance cues and related mechanisms in proper CC development. In FASD, complete/partial absence of the CC is apparent along with other anomalies. Research shows that alcohol exposure affects Netrin-1/DCC gene expression. Because of this and other strong similarities between FASD and phenotypes including axon guidance mutants, prenatal alcohol exposure likely affects axon guidance mechanisms that result in abnormal CC development. Though little research exists on which mechanisms are specifically affected by alcohol, we are able to conjecture and suggest future research that would help to understand the specifics of how dangerous alcohol can be to the developing brain.

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