Where Did the Myelin Go? Determining the Mechanism by which Alcohol Drinking Reduces Myelin in Adolescence

Presenter

Jayden Amirault

Campus

UMass Amherst

Sponsor

Heather Richardson, Department of Psychological and Brain Sciences, UMass Amherst

Schedule

Session 5, 3:30 PM - 4:15 PM [Schedule by Time][Poster Grid for Time/Location]

Location

Poster Board A59, Campus Center Auditorium, Row 3 (A41-A60) [Poster Location Map]

Abstract

It is estimated that 34.4% of people ages 12 to 20 reported having at least one drink in their lives, with 8.3% of this group reporting binge-drinking within the past month. Binge drinking is defined as drinking enough alcohol to exceed a blood alcohol concentration of 0.08% within 2 hours. Binge drinking during adolescence leads to decreased myelin in the prefrontal cortex, and specifically in the anterior branches of the corpus callosum. Myelin is the fatty sheath that covers axons, and it is important for faster signaling. The mechanism underlying this loss in myelin is not well understood. We used a transgenic mouse model that allows us to control the expression of membrane bound green fluorescent protein (mGFP). This combined with immunohistochemical labeling of a myelin sheath protein allows us to distinguish between myelin that is added to axons before adolescence versus myelin that is added during and after adolescence. By comparing myelin between mice that consumed alcohol and mice that consumed water, we can test if alcohol-induced myelin deficits are caused by demyelination, interference of new myelin being formed (myelinogenesis), or by a combination of both factors. Identifying the mechanisms and molecular targets to test in follow up experiments can provide groundwork for the development of new clinical interventions aimed at combating and reversing effects of binge alcohol use in adolescent and long term adult users.

Keywords

Myelin, alcohol binge drinking, adolescence, prefrontal cortex, Mouse model

Research Area

Neuroscience and Cognitive Science

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