The effect of a Ring A-reduced metabolite of corticosterone, 5 alpha-dihydrocorticosterone (DHB) on long-term potentiation (LTP) in the dentate gyrus (DG) of the rat were studied in barbiturate-anaesthetised animals. It was observed that DHB significantly impairs the development of LTP, more particularly the population spike (PS) component of the evoked potential (EP) to perforant path (PP) stimulation. Nutralipid, an inert control solvent of the steroid, did not affect LTP development. We argue that both, membrane and intracellular effects of DHB, are involved in the mechanisms responsible for DHB blocking of LTP.