Researcher(s)
- Kaitlyn Goblirsch, Neuroscience, University of Delaware
Faculty Mentor(s)
- Anna Klintsova, Psychology and Brain Sciences, University of Delaware
Abstract
Fetal alcohol spectrum disorders (FASDs) is an umbrella term for diagnoses resulting from prenatal alcohol exposure (AE) and characterized by behavioral, physical, and cognitive deficits, including deficits in executive functioning. Previous research in our lab revealed the midline thalamic nucleus reuniens (Re), a key component of the executive functioning circuit, to be damaged by AE during a period in development known as the Brain Growth Spurt (BGS). BGS occurs in the third trimester of human gestation and during the first two postnatal weeks in rats, allowing us to model AE in these animals. Previous results from our lab have shown an increase in cell death shortly after one day of moderate (3g/kg/day) or high (5g/kg/day) AE on postnatal day 9 (PD9), but these effects did not translate into loss of cells in adulthood.
My summer project focused on the effects of single-day binge AE during the BGS on populations of neurons and astrocytes in the Re in adulthood. Rat pups were divided into three groups on PD9: moderate AE (3g/kg/day), high AE (5.25g/kg/day), and sham intubation (procedural controls), with 6 animals per condition per sex. Alcohol mixed with milk formula was given via intragastric intubation. The animals were weaned on PD23 and socially housed with 2 same-sex animals per cage. Animals were anesthetized, perfused, and brain tissue was collected on PD65.
The brains were sectioned in coronal plane at 40 μm on a cryostat and then stained immunohistochemically with primary antibodies against glial fibrillary acidic protein (GFAP), a specific protein expressed in astrocytes, and NeuN, a neuronal marker. Series of images through the extent of Res were collected using epifluorescent microscope and StereoInvestigator software to estimate the number of neurons and astrocytes in control and AE brains. Tissue analysis is underway.