Although it has been established that recurrent or prolonged clinical seizures 
during infancy may cause lifelong brain damage, the underlying molecular 
mechanism is still not well elucidated. The present study, to the best of our 
knowledge, is the first to investigate the expression of twenty zinc (Zn)/lipid 
metabolism‑associated genes in the hippocampus and cerebral cortex of rats 
following recurrent neonatal seizures. In the current study, 6‑day‑old 
Sprague‑Dawley rats were randomly divided into control (CONT) and recurrent 
neonatal seizure (RS) groups. On postnatal day 35 (P35), mossy fiber sprouting 
and gene expression were assessed by Timm staining and reverse 
transcription‑quantitative polymerase chain reaction, respectively. Of the 
twenty genes investigated, seven were significantly downregulated, while four 
were significantly upregulated in the RS group compared with CONT rats, which 
was observed in the hippocampus but not in the cerebral cortex. Meanwhile, 
aberrant mossy fiber sprouting was observed in the supragranular region of the 
dentate gyrus and Cornu Ammonis 3 subfield of the hippocampus in the RS group. 
In addition, linear correlation analysis identified significant associations 
between the expression of certain genes in the hippocampus, which accounted for 
40% of the total fifty‑five gene pairs among the eleven regulated genes. 
However, only eight gene pairs in the cerebral cortex exhibited significant 
positive associations, which accounted for 14.5% of the total. The results of 
the present study indicated the importance of hippocampal Zn/lipid 
metabolism‑associated genes in recurrent neonatal seizure‑induced aberrant mossy 
fiber sprouting, which may aid the identification of novel potential targets 
during epileptogenesis.