Extra- and intracellular recordings in slices were used to examine what types of synaptic plasticity can be found in the core of the nucleus accumbens, and how these forms of plasticity may be modulated by dopamine. Stimulus electrodes were placed at the rostral border of the nucleus accumbens in order to excite primarily infralimbic and prelimbic afferents, as was confirmed by injections of the retrograde tracer fluoro-gold. In extracellular recordings, tetanization induced long-term potentiation (LTP) of the population spike in 20 out of 53 slices. The presynaptic compound action potential did not change following LTP induction. For the intracellularly recorded excitatory postsynaptic potentiation, three types of synaptic plasticity were noted: long-term potentiation (16 out of 54 cells), decremental potentiation (eight cells) and long-term depression (LTD; six cells). No correlation was found between the occurrence of potentiation or depression and various parameters of the tetanic depolarization (e.g. peak voltage, integral under the curve). The N-methyl-D-aspartate receptor antagonist D(-)-2-amino-5-phosphonopentanoic acid (50 microM; D-AP5) reduced, but did not completely prevent, the induction of LTP. The incidence of LTD was not markedly affected by D-AP5. No difference in LTP was found when comparing slices bathed in dopamine (10 microM) and controls. Likewise, slices treated with a mixture of the D1 receptor antagonist Sch 23390 (1 microM) and the D2 antagonist S(-)-sulpiride (1 microM) generated a similar amount of LTP as controls. In conclusion, both LTP and LTD can be induced in a key structure of the limbic-innervated basal ganglia. LTP in the nucleus accumbens strongly depends on N-methyl-D-aspartate receptor activity, but is not significantly affected by dopamine.