Purpose Many of the short and long term consequences of epilepsy may be due to excitotoxicity, of which protein nitrosylation is a central feature. Levels of 3-nitrotyrosine (3NT) are raised in other neurological diseases, and known to have key functional consequences. We have already shown that 3NT is raised in rat brain following seizures (novel finding). We set out to establish the time course of this change. Methods Self-sustaining SE (perforant path model) was induced for 3 hours, then terminated with diazepam. 7 days later, the rats were decapitated under anaesthesia, the hippocampal subregions dissected on ice, and snap frozen. Sham controls underwent identical procedures, with the exception of electrical stimulation. 3NT was quantified using high performance liquid chromatography with electrochemical detection. Results Mean hippocampal 3NT levels (expressed as a ratio to L-tyrosine) were not different in status animals (3.27×10-5+/-3.96×10-6SEM) compared with controls (3.75×10-5+/-1.02×10-5SEM). Subregional analysis confirmed this finding in the dentate gyrus/hilar (DG/H) region (SE 3.48×10-5+/-5.23×10-6, sham 4.29×10-5+/-1.86×10-5), CA1 (SE 2.98×10-5+/-1.06×10-6, sham 2.03×10-5+/-5.36×10-6) and CA3 (SE 3.36×10-5+/-4.56×10-6, sham 4.92×10-5+/-2.46×10-5) regions. Conclusions This study is the first to describe the time course of changes in 3NT expression following seizures in a rat model of epilepsy, and has implications for our understanding of the morbidity of seizures. Further studies are required to understanding the functional localization and consequences of protein nitrosylation following SE.