NMDA receptor (NMDA-R) in the amygdala complex is critical for both long-term potentiation (LTP) and formation of conditioned fear memory. It is reported that activation of β-adrenoceptors (β-AR) in the amygdala facili-tates LTP and enhances memory consolidation. The present study examined the regulatory effect of β-AR activation on NMDA-R mediated current in pyramidal cells of the baso-lateral nucleus of amygdala (BLA), using whole-cell re-cording technique. Bath application of the β-AR agonist iso-proterenol enhanced NMDA-induced current, and this fa-cilitatory effect was blocked by co-administered propranolol, a β-AR antagonist. The facilitatory effect of isoproterenol on NMDA-induced current could not be induced when the pro-tein kinase A (PKA) inhibitor Rp-cAMPs was added in elec-trode internal solution.The present results suggest that β-AR activation in the BLA could modulate NMDA-R activity di-rectly and positively, probably via PKA. The NMDA receptor (NMDA-R) in the amygdala complex is critical for both long-term potentiation (LTP) and formation of conditioned fear memory. It is reported that activation of β-adrenoceptors (β-AR) in the amygdala facili-tates LTP and enhances memory consolidation. The present study examined the regulatory effect of β-AR activation on NMDA-R mediated current in pyramidal cells of the baso-lateral nucleus of amygdala (BLA), using whole-cell re-cording technique. Bath application of the β-AR agonist iso-proterenol enhanced NMDA-induced current, and this fa-cilitatory effect was blocked by co-administered propranolol, a β-AR antagonist. The facilitatory effect of isoproterenol on NMDA-induced current could not be induced when the Pro-tein kinase A (PKA) inhibitor Rp-cAMPs was added in elec-trode internal solution. The present results suggest that β-AR activation in the BLA could modulate NMDA-R activity di-rectly and positively, probably via PKA.