We have investigated the role of cortico-cortical inputs from the primary somatosensory cortex in the induction of long-lasting potentiation in the secondary somatosensory cortex. Long-lasting potentiation of evoked potentials in the feline secondary somatosensory cortex is induced by high frequency stimulation of the ventral posterolateral thalamic nucleus. The secondary somatosensory cortex receives two projections from the ventral posterolateral thalamic nucleus; a direct pathway from the ventral posterolateral thalamic nucleus and a cortico-cortical pathway via the primary somatosensory cortex. The present study was designed to examine dominance of these pathways in the induction of long-lasting potentiation in the secondary somatosensory cortex. Long-lasting potentiation was evaluated by changes in the amplitude of field potentials and current source densities elicited by ventral posterolateral thalamic nucleus test stimulation (0.1 Hz) following conditioning stimulation. The conditioning stimulation, consisting of 20 trains of 200 Hz bursts, was delivered to the ventral posterolateral thalamic nucleus or the primary somatosensory cortex. Field potentials in the secondary somatosensory cortex were simultaneously recorded at 16 points placed vertically at 150 microns intervals from the cortical surface and current source density was computed using these field potentials. First, we blocked inputs from the primary somatosensory cortex to the secondary somatosensory cortex by intracortical injection of lidocaine into the primary somatosensory cortex. The amplitudes of the field potentials recorded in the secondary somatosensory cortex diminished within 5 min after lidocaine injection. Current source density analysis showed a marked decrease in the sink currents in layers II/III (at depths of 450-600 microns).(ABSTRACT TRUNCATED AT 250 WORDS)