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INTRODUCTION: Temporal lobe epilepsy develops as a consequence of brain insults such as trauma, stroke, infection, or seizures. The temporal lobe circuit, including the hippocampus, reorganizes generating hyperexcitable networks and, therefore, the epileptic focus, process called epileptogenesis. Whereas, the cerebral cortex is more resistant to the reorganization. Temporal lobe epileptogenesis is mediated partly by neuronal nitric oxide synthase and the neurotrophin BDNF with its receptor TrkB. These proteins are localized at excitatory synapses and might be involved in the differential sensitivity of the hippocampus and cerebral cortex to epileptogenesis. OBJECTIVE: Getting closer to mechanisms involved in epileptogenesis differential sensitivity between the hippocampus and cortex after seizures. MATERIAL AND METHOD: Seizures were induced in rats by injection of kainic acid. Resealed synaptic membranes (synaptosomes) were obtained from cortex and hippocampus. Then the co-localization of neuronal nitric oxide synthase, TrkB and a marker of excitatory synapses (Prosap2/Shank3) was quantified by immunohistochemistry. The results were expressed as mean ± standard error and subjected to t-student test. RESULTS: TrkB and neuronal nitric oxide synthase increased from 20.6 ± 3.5% to 35.7 ± 2.6% (p = 0.0008) and from 32.4 ± 3.8% to 51.5 ± 3.5 % (p = 0.0003), respectively in excitatory hippocampal synaptosomes after seizures. In excitatory cerebrocortical synaptosomes no significant changes were observed. DISCUSSION: neuronal nitric oxide synthase and TrkB associate to excitatory hippocampal synapses after seizures, thereby probably contributing to epileptogenesis. The cerebral cortex is resistant to this molecular reorganization. [ABSTRACT FROM AUTHOR]