Possible involvement of the amygdaloid input in long-term potentiation (LTP) in the medial perforant path-dentate gyrus granule cell synapses in vivo was investigated by evaluating the effects of lesions of the amygdaloid nucleus. The dentate gyrus synaptic potential evoked by low-frequency test stimulation did not change following lesions of the basolateral and central amygdala. However, when tetanic stimulation (30 pulses at 60 Hz) was applied 60 min after lesioning of the ipsilateral basolateral amygdala, the magnitude of LTP was significantly attenuated. Since lesions of the ipsilateral central amygdala and the contralateral basolateral amygdala did not affect the dentate gyrus LTP, the attenuation of the dentate gyrus LTP is a specific effect of acute lesions of the ipsilateral basolateral amygdala. The basolateral amygdaloid lesions significantly attenuated both LTP induced by weak (20 pulses at 60 Hz) and strong (100 pulses at 100 Hz) tetanus, indicating that the effect of the lesions does not depend on the strength of tetanus applied to induce LTP. When the ipsilateral basolateral amygdala was destroyed after application of tetanus, it did not affect the established LTP. The attenuation of LTP was also observed after the basolateral amygdala-lesioned rats were allowed a recovery period of 2 weeks. This is the first report providing evidence that the ipsilateral basolateral amygdala modulates hippocampal synaptic plasticity in vivo.