Researcher(s)
- Grace Lyons, Neuroscience, University of Delaware
Faculty Mentor(s)
- Anna Klintsova, Psychological and Brain Sciences, University of Delaware
Abstract
Fetal alcohol spectrum disorders (FASD) can result from prenatal alcohol exposure (AE). One of the most prevalent cognitive symptoms of FASD is impaired executive function (EF). EF is reliant on the circuitry that involves medial prefrontal cortex, hippocampus and structures in the midline thalamic region. Inhibitory action in the thalamus is driven by the thalamic reticular nucleus (TRN), as the TRN contains a high presence of PV+ inhibitory interneurons. The majority of PV+ interneurons in TRN are surrounded by perineuronal nets (PNNs) – a component of the extracellular matrix (ECM). PNNs are important in maintaining the excitatory/inhibitory (E/I) balance and for synaptic stabilization, and are vulnerable to insults during development, including brain growth spurt. Current research in Klintsova’s lab aims to establish the AE-related damages to the TRN using a rat model of exposure in the third trimester. Specifically, my project investigates how alcohol affects the presence of PNNs at different points in development.
Previously generated brains of Long Evans rat pups were used in the study. Rat pups were administered 2 doses of alcohol on a single postnatal day (PD) 9 or were sham intubated (SI). Pups were intracardially perfused on PD9, PD15, or PD65 and brains were postfixed. Brains were sectioned in a coronal plane and immunostained using biotinylated Wisteria Floribunda Agglutinin (WFA) and DAB-Ni enhanced solution to visualize PNNs. Images of the entire hemisphere containing the TRN were acquired. The region of interest will be outlined and the optical density of the region will be measured using ImageJ software. The study is ongoing and data will be used in a senior thesis project examining expression of PNNs in the TRN at various time points after alcohol exposure. We hypothesize that developmental AE will reduce PNN density in the TRN, resulting in the altered excitatory/inhibitory balance in the thalamus.