Loss of consciousness during focal limbic seizures significantly contributes to reduced quality of life for people with epilepsy (Vickrey et al., 2000). Previous work has established the network inhibition hypothesis, which posits that focal limbic seizures impair arousal through inhibition of subcortical structures, causing sleep-like, low-frequency cortical oscillations and impaired consciousness (Blumenfeld, 2021). Inhibited brainstem and basal forebrain cholinergic, serotonergic as well as putative glutamatergic thalamic signaling have previously been implicated as contributing pathways for depressed arousal in rat focal limbic seizures (Englot et al., 2008; Feng et al., 2017; Motelow et al., 2015; Zhan et al., 2016). A recent novel, awake, head-fixed mouse model demonstrated impaired behavioral responsiveness and cortical slow waves resembling human temporal lobe seizures, along with reduced cortical cholinergic neurotransmission (Sieu et al., 2024). However, the role of norepinephrine (NE) and the locus coeruleus (LC) during ictal unconsciousness has not been studied in detail. The LC-NE system is a target of interest in this context as it has been shown to have bilateral projections both to the limbic system and the frontal cortex (Room et al., 1981), has long been associated with the regulation of arousal and plays a significant role in sleep-wake transitions. For example, in awake mice optogenetic inhibition of LC increased cortical slow-wave activity and induced slow wave sleep (Carter et al., 2010). A recent study of LC neurons in anesthetized rats showed variable changes in neuronal activity during hippocampal seizures related to the location of neurons in the LC (Larsen et al., 2023). Therefore, our goal was to investigate the potential role of the LC-NE system in decreased ictal arousal in an awake behaving mouse model of focal temporal lobe seizures, and to determine if activity in this arousal system is decreased, as would be predicted by the network inhibition hypothesis (Blumenfeld, 2021). To this end, electrophysiology recordings in an awake, behaving mouse model were employed (Sieu et al., 2024). Better understanding of these pathways is critical to identify potential targets for therapeutic intervention.