Impaired cognitive control after moderate prenatal alcohol exposure corresponds to altered EEG power during a rodent touchscreen continuous performance task

Abstract

Although it is well established that alcohol consumption during pregnancy can lead to lifelong difficulties in offspring, Fetal Alcohol Spectrum Disorders (FASD) remain a common neurodevelopmental syndrome. Translational behavioral tools that target similar brain circuits across species can facilitate understanding of these cognitive consequences. Touchscreen behavioral tasks for rodents enable easy integration of dura recordings of electroencephalographic (EEG) activity in awake behaving animals, with clear translational generalizability. Recently, we showed that Prenatal Alcohol Exposure (PAE) impairs cognitive control on the touchscreen 5-Choice Continuous Performance Task (5C-CPT) which requires animals to touch on target trials (hit) and withhold responding on non-target trials (correct rejection). Here, we extended these findings to determine whether dura EEG recordings would detect task-relevant differences in medial prefrontal cortex (mPFC) and posterior parietal cortex (PPC) corresponding with behavioral alterations in PAE animals. Replicating previous findings, PAE mice made more false alarm responses versus controls and had a significantly lower sensitivity index. All mice, regardless of sex or treatment, demonstrated increased frontal theta-band power during correct trials that followed an error (similar to post-error monitoring commonly seen in human participants). All mice showed a significant decrease in parietal beta-band power when performing a correct rejection versus a hit. PAE mice of both sexes showed a significantly larger decrease in parietal beta-band power when successfully rejecting non-target stimuli. These findings suggest that moderate exposure to alcohol during development can have long lasting effects on cognitive control, and task-relevant neural signals may provide a biomarker of impaired function across species.