Rationale: Absence seizures are generalized non-motor epileptic seizures characterized by recurrent spontaneous five- to ten-second episodes of unresponsiveness, with distinct rhythmic 3-4Hz spike-and-wave discharges (SWDs) on electroencephalogram (EEG). In animal models of absence seizures, behavioral responses to conditioned auditory stimuli have been shown to be impaired during SWDs. The mechanisms disrupting the ascending auditory pathway process remain unclear, although spared cortical sensory responses have been shown in the primary sensory areas of animal models under anesthesia. The purpose of this study was to investigate changes in sensory auditory input processing in the primary auditory cortex during SWDs in the Genetic Absence Epilepsy Rats from Strasbourg (GAERS) awake model. Methods: GAERS aged four to eight months were food restricted and trained to a conditioned tone response task, which involved licking a spout for a sucrose reward following a 0.5 auditory stimulus. Neuronal activity was recorded with multi-channel silicon ensemble recordings in the primary auditory cortex (A1) and SWDs were detected by an epidural EEG electrode over the somatosensory barrel cortex (S1). Signals were recorded with Intan amplifiers and an Open Ephys recording system. Results: Cortical auditory evoked potentials in response to an auditory stimulus were similar during baseline wakefulness and during SWDs. In addition, the average root-mean-square multi-unit activity time course in response to an auditory stimulus showed similar onset and offset responses during baseline wakefulness and during SWD. Rats were more likely to respond correctly to the auditory stimulus during baseline conditions compared to during SWDs. Conclusions: These findings suggest that behavioral impairment involving sound inputs during SWDs are likely not due to a disruption in primary sensory auditory transmission. We plan to investigate additional processing areas in the auditory sensory – motor transduction pathway to determine at what stage signals are disrupted by SWD to produce impaired behavioral responses. Funding: Please list any funding that was received in support of this abstract.: NIH R37NS100901, Foundation of Anesthesia Education and Research (FAER) Mentored Research Training Grant, NIH Clinical and Translational Science Award (CTSA) Grant number UL1 TR001863 from the National Center for Advancing Translational Science (NCATS).