Document Type
Poster
Publication Date
2022
Abstract
Fetal alcohol exposure is a pervasive cause of intellectual disability. The range of effects caused by prenatal ethanol exposure are grouped under the umbrella term, Fetal Alcohol Spectrum Disorders (FASDs). Exposure to alcohol during any period of pregnancy can damage the fetal brain, including the last trimester of pregnancy, where the brain growth spurt takes place. Ethanol exposure during late pregnancy produces learning and memory deficits that can last into adulthood. Studies suggest that these deficits may be a consequence of damage to the posterior limbic memory system. This system includes specialized neuronal populations in several connected regions: the subiculum, retrosplenial cortex, mammillary bodies and anterior thalamic nuclei. Research from multiple laboratories has demonstrated that binge-like ethanol exposure during the third trimester equivalent of human gestation activates apoptotic pathways in these brain regions. We hypothesized that this would result in a long-lasting reduction of neuronal numbers in the anterior thalamic nuclei. To test this hypothesis, we exposed VGAT-Venus mice (expressing fluorescently tagged GABAergic interneurons) at postnatal day 7 (P7) to heavy, binge-like ethanol in vapor chambers (blood ethanol level ~0.4 g/dl; ~90 mM). Pups were left undisturbed until adolescence (~P60-70) when their brains were processed for immunohistochemistry with an antibody against the neuron-specific antigen, NeuN. Neuronal numbers were quantified exhaustively in a blind fashion, in images obtained with a Nuance spectral imaging system, using the point selection tool in Fiji (NIH Image J software). We found that ethanol exposed mice reduced neuronal numbers in the anterior dorsal, anterior ventral, and thalamic reticular nuclei of male but not female mice. Ongoing studies are investigating whether surviving anterior thalamic neurons display functional alterations that contribute to the persistent learning and memory deficits caused by binge-like ethanol exposure during the mouse equivalent to the last trimester of human pregnancy.
Recommended Citation
Mayfield, Stephanie; G Jill Chavez; Clark Bird; and C Fernando Valenzuela. "Third Trimester-Equivalent Ethanol Exposure Decreases Neuronal Numbers in the Antero-Ventral and Reticular Nuclei of the Thalamus of Adolescent Male Mice." (2022). https://digitalrepository.unm.edu/hsc-bbhrd/56
Comments
Poster presented at the Brain & Behavioral Health Research Day 2022