Impact of Developmental Alcohol Exposure on the Thalamus.

This chapter comprehensively explores the impact of prenatal alcohol (ethanol) exposure (PAE) on the thalamus, integrating findings from animal models and human studies spanning various developmental stages. Animal model investigations, encompassing first and second trimester-equivalent exposures and the critical third trimester, where the brain growth spurt starts, reveal specific alterations in thalamic structures and circuits, emphasizing the specificity of damage to corticothalamic loops. The ventrobasal thalamic nucleus exhibits a unique response to PAE, involving intricate interactions with postnatal neurogenesis and neurotrophin responsiveness. Third trimester-equivalent exposure consistently induces apoptotic neurodegeneration in various thalamic nuclei, highlighting the heightened susceptibility of the visual thalamus, particularly the lateral geniculate nucleus, during critical developmental periods. The nucleus reuniens, vital for cognitive processes, was shown to be significantly affected by alcohol exposure during this period. Investigations into the trigeminal/somatosensory system activity revealed disruptions in glucose utilization and increased neuronal activity in the thalamus. Research on binge-like alcohol exposure during the brain growth spurt demonstrates lasting modifications in action-potential properties and synaptic currents in thalamic neurons projecting to the retrosplenial cortex. Human studies, employing advanced techniques like super-resolution fetal MRI and functional MRI, underscore the PAE-induced structural and functional consequences in the thalamus and its connections, spanning from fetal development to adulthood. The complex effects of PAE on thalamic structure and function vary across developmental stages, emphasizing the importance of considering factors such as age and concurrent exposures. The development of higher-resolution imaging tools is essential for assessing the impact of PAE on the structure and function of individual thalamic nuclei in humans.