Defining prenatal alcohol exposure impact on frontoparietal signaling during cognitive control

The National Institute on Alcohol Abuse and Alcoholism (NIAAA) awarded the University of New Mexico Health Sciences Center $160,744 on March 9, 2026, under the Alcohol Research Programs (CFDA 93.273) to investigate electrophysiological mechanisms of prenatal alcohol exposure (PAE) effects on cognitive control.

The project combines translational touchscreen testing and in vivo electrophysiology to determine how PAE impairs executive function domains in mouse models. The research hypothesizes that PAE reduces parvalbumin fast-spiking interneurons in the posterior parietal cortex, disrupting the ability to gate excitatory signaling in frontoparietal circuits necessary for cognitive control. Electrodes will be implanted in the posterior parietal cortex and medial prefrontal cortex to collect data during a five-choice continuous performance task assessing executive function. Analytic tools will measure PAE's impact on excitatory/inhibitory balance, oscillatory signaling, and synchronous activity between the two brain regions.

The award funds work performed in New Mexico with a period of performance through December 31, 2030. This Project Grant falls under NIAAA's mission to develop a sound knowledge base supporting improved treatment methods and prevention strategies for alcoholism and alcohol-related problems, with support typically not exceeding five years.

Abstract

Consumption of alcohol during pregnancy results in the development of fetal alcohol spectrum disorders (fasd), which is conservatively estimated to affect 5% of united states first graders. Individuals with fasd often report difficulties with executive function domains including cognitive control, which is the ability to maintain goal-directed behavior despite distractions. Such cognitive control deficits have been replicated in mouse models of prenatal alcohol exposure (PAE); however, the electrophysiological underpinnings of these deficits are not understood. To fill this knowledge GAP, i propose to investigate the underlying electrophysiological mechanism(s) of PAE-associated cognitive control deficits by combining translational touchscreen testing and in vivo electrophysiology with a first- and second-trimester equivalent moderate PAE paradigm. My central hypothesis is that PAE induces long-term impairments in cognitive control by reducing parvalbumin fast-spiking interneurons in the posterior parietal cortex (PPC), which results in an inability to gate incoming excitatory signaling in frontoparietal circuits required to exert cognitive control. Electrodes will be implanted into the PPC and medial prefrontal cortex (mpfc), allowing data collection during the 5 choice continuous performance task (5C-CPT). 5C-CPT is a translational touchscreen paradigm that assesses many domains of executive function, including cognitive control. Multiple analytic tools will be used to investigate the impact of PAE on the excitatory/inhibitory balance and oscillatory signaling of the PPC. Additional tools will be used to determine if PAE dysregulates frontoparietal signaling via decreases in synchronous activity between the mpfc and PPC. Collectively, this proposal will determine the impact of PAE on electrophysiological functions in both the PPC alone and the mpfc-PPC reciprocal circuitry during trials taxing cognitive control. The successful completion of this proposal will provide crucial information on the lasting neurological impacts of moderate PAE on individual neurons and oscillations in both the PPC and the reciprocal mpfc-PPC circuitry. Additionally, this work will provide intensive training in awake-behaving high-yield electrophysiology, translational touchscreen behavior, and complex data analysis.