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EPILEPTIFORM DISCHARGES AS A POTENTIAL MECHANISM OF MEMORY DISRUPTIONS FOLLOWING THIRD-TRIMESTER ALCOHOL EXPOSURE
Abbey Myrickand 3 co-authors
University of New Mexico
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS06-09PM-076
Presentation
Date TBA
Board: PS06-09PM-076
Event Information
Poster Board
PS06-09PM-076
Poster
View posterAbstract
Third Trimester Alcohol Exposure (TTAE) damages the Hippocampal-Retrosplenial Cortical Circuit (HRCC) - a critical neural pathway for learning and memory that propagates information via High Frequency Oscillations (HFOs). Changes in HRCC function are therefore speculated to drive differences in learning and memory observed in certain individuals with prenatal alcohol exposure. In the current study using a mouse model of TTAE, we unexpectedly discovered epileptiform discharges - pathological events associated with epilepsy and neurodegeneration - and assessed their impact on HFOs. Male and female TTAE and control (saline) mice were produced using a single day, double alcohol injection model (5 g/kg total) at postnatal day 7. After postnatal day 60, electrodes were implanted into the retrosplenial cortex and hippocampus and home cage electrophysiological recordings were collected in 24-hour epochs. Epileptiform discharges occurred most frequently during Non-Rapid Eye Movement (NREM) sleep. We also observed a remarkable increase in HFOs within the retrosplenial cortex immediately following epileptiform discharges (100ms), whose duration and frequency was negatively correlated with time post-event. Additionally, we discovered temporal differences in epileptiform discharge arrival time between the retrospenial cortex and hippocampus, suggesting multiple pathways within the larger HRCC circuit. Importantly, mice did not exhibit outward symptoms of epileptic activity. These results identify and characterize HRCC epileptiform discharges as a potential mechanism for learning and memory differences through the disruption of memory consolidation during NREM.
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