Aims: Interleukin-1β (IL-1β) in the central nervous system initiates a PI3K signaling cascade, involving crucial membrane phospholipids phosphatidylinositol (4,5)-bisphosphate (PIP2) and phosphatidylinositol (3,4,5)-trisphosphate (PIP3). While PIP2's role in epileptogenesis is known, our study investigates the unclear role of PIP3 using PTZ-induced epileptic mice, exploring its impact on epileptogenesis and associated sleep disruptions. Methods: Our hypothesis proposed a pivotal role for PIP3 in the molecular mechanism of seizures. We intraperitoneal administered low dose of PTZ once every two days for seven injections to induce spontaneous recurrent seizures in mice. We distinguished the differences between IL-1R1 knockout (KO) and wild-type mice in seizure generation and sleep-wake patterns. Additionally, we employed various inhibitors to block specific signaling pathways to further prove our hypothesis. Results: Our results highlighted the importance of IL-1β and PIP3 in epileptogenesis, suggesting potential interventions to alleviate PTZ-induced seizures and associated sleep disruptions. Protein expression analysis revealed notable changes in interaction protein for cytohesin exchange factors 1 (IPCEF1) and NMDA receptor (NMDAR) subunits. Sleep data demonstrated alterations in sleep architecture due to epileptic activity, indicating a link between the IL-1/PIP3/AKT signaling pathway and sleep disturbances in epilepsy. Conclusion: Our study suggests that PTZ kindling increases IPCEF1 and NR1 expression. Interestingly, using inhibitors and antagonists mitigated the increase induced by PTZ. These results further validated the involvement of the IL-1/PIP3/AKT signaling pathway and highlighted the significance of PIP3 in epilepsy.