The distribution and morphology of neuronal degeneration were observed and analyzed in each sector of the zona incerta in a lithium‑pilocarpine (LiCl) Wistar rat model of status epilepticus in 12, 15, 18, 21, and 25‑day‑old rats and survival intervals of 4, 8, 12, 24, and 48 hours. Status epilepticus was induced via intraperitoneal (IP) injection of LiCl (3 mmol/kg) 24 hours before an injection of pilocarpine (40 mg/kg, IP). Motor seizures were suppressed by paraldehyde (0.3‑0.6 ml/kg, IP) two hours after status epilepticus onset. Animals were anesthetized using urethane and perfused with phosphate‑buffered saline followed by 4% paraformaldehyde. Brains were sectioned and Nissl stained for map guidance, with fluoro‑Jade B fluorescence used to detect degenerated neurons. Fluoro‑jade B‑positive neurons were plotted to a standard stereotaxic atlas, their distribution was quantified, and their long‑axis diameter was measured. Fluoro‑jade B‑positive neurons were found in pups aged 15 days and older 24 hours after status epilepticus, in which their numbers increased, and their perikaryon size decreased with advancing age. Thus, neuronal damage severity was dependent on age and survival interval. Neuronal damage was only found in the rostral sector of the zona incerta, a region that exhibits a small number of inhibitory neurons and is reciprocally connected to the limbic cortex. This system of hyperactivity, coupled with inhibitory neurons, may be the underlying cause of the neuronal degeneration and explain why it was confined to the rostral sector of the zona incerta.