Long-term potentiation (LTP) was induced in the dentate gyrus of freely moving rats by tetanic stimulation of the medial entorhinal cortex under conditions of catecholamine depletion by 200 mg/kg alpha-Methyl-para-tyrosine (AMPT) or blockade of alleged dopamine receptors by 0.5 mg/kg haloperidol. Both substances did not change significantly the normal excitability of the glutamatergic perforant pathway, but affected the establishment of LTP. Whereas the potentiation effect on the EPSP component of the monosynaptic field potential was not changed by both substances when compared to the potentiation of controls, the potentiation of the population spike was prolonged and enhanced. These results point to an effect of catecholaminergic blockade on postsynaptic membranes of the target cells or on other components of the neuronal network but not to a specific influence on the homosynaptic mechanisms of LTP.