We investigated the neuroprotective efficacy of hypothermia after status epilepticus (SE) in immature rats. In addition, the expression levels of NMDAR1 and c-Jun were measured to establish a possible signaling mechanism for hypothermia-induced neuroprotection. Pilocarpine-treated rats were randomly divided into 2 groups: group D (diazepam) and group DH (diazepam plus hypothermia). Compared to the control (group NS) rats, Pilocarpine-induced SE significantly enhanced the expression of NMDAR1 and c-Jun in the hippocampus, and also significantly increased the numbers of necrotic and apoptotic pyramidal neurons. The DH group exhibited significantly fewer necrotic and apoptotic hippocampal pyramidal neurons and reduced NMDAR1 expression than group D. In contrast, early expression of c-Jun was significantly higher in the hippocampi of hypothermia-treated rats than in the hippocampi of group D, while late c-Jun expression was significantly lesser than group D. Our results show mild post-ictal hypothermia partially rescues neuronal cell death in the hippocampus following SE. We further suggest that elevated NMDAR1 expression exacerbates SE-induced neuronal death in pilocarpine-treated rats, while early c-Jun overexpression, concomitant with hypothermia, suppresses subsequent neuronal death.