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The effects of exogenous application of excitatory amino acids on synaptic transmission was investigated in the CA1 region of the rat hippocampal slice preparation using two methods of application: iontophoresis and perfusion. Iontophoretic application of N-methyl-D-aspartate (NMDA) evoked a short lasting form of potentiation, whereas application of the proposed endogenous excitatory transmitter substance L-glutamate induced a slowly-forming and long lasting potentiation of the response by both techniques. Surprisingly, brief perfusion of 50μM NMDA elicited only a long-lasting depression of the response. Application of 10μM α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) showed no long-term effects on synaptic transmission. Perfusion of (1S,3R) 1-aminocyclopentane-1,3-dicarboxylic acid (ACPD) induced only a marginal form of synaptic enhancement under normal conditions and depression of the response in conditions of low Mg2+ or in the presence of low doses (1μM) of picrotoxin. However, in the presence of the GABAA antagonist picrotoxin (1μM), perfusion of 100μM ACPD evoked a slowly-forming enhancement of the response. Application of the proposed retrograde transmitter arachidonic acid (10μM) elicited a slowly-forming depression of the response when perfused alone. Co-application of arachidonic acid (10μM) and ACPD (50μM) evoked a rapidly inducible and long-lasting form of synaptic enhancement.