Activation of expression of genes encoding components of AP-1 transcription factor (c-fos, c-jun and their cognates) as well as AP-1 itself has been repeatedly shown to coincide with long-term cellular responses. For the proliferating cells where functional involvement of AP-1 in physiological activity has been proved, cellular senescence as well as aging at level of the organism results in an alteration of the AP-1. The aim of the present study was to analyze whether there is an aging-related defect in the formation of AP-1 transcription factor in the brain. AP-1 has been shown previously to be inducible by several stimuli in the cells of the central nervous system, including proconvulsant treatment of pentylenetetrazole (PTZ). The present studies found that PTZ robustly induced AP-1 DNA binding activity, evaluated by the electrophoretic mobility shift assay, in hippocampi of aged (2-year-old) rats, indicating no aging-related AP-1 defect in the rat brain.