The Role Of The Amygdala Basolateral Nucleus Of ¦Â Receptors In Fear Conditioning Sound

The present study examined whether β-adrenoceptor (β-AR) in the basolateral nucleus of amygdala ( BLA) is involved in memory consolidation of auditory fear conditioning. Rats were placed in chamber A and presented with a 30-s auditory cue (CS) . During the last 2s of the CS, rats were delivered with an electric shock to foot (US). The β-AR antagonist L-propranolol (10μg each side) was infused bilaterally into the BLA 0h or 6h after conditioning. Rats were tested for memory retension 24h later. Results show that infusion of L-propranolol 0h post-training impaired 24-h memory retention, whereas infusion of L-propranolol 6h after conditioning had no effect. Control experiments show that L-propranolol interfered with long-term memory (LTM ) , but not short-term memory (STM) . The present results indicate that β-AR in BLA is essential for memory consolidation of auditory fear conditioning.The present study investigated if β-adrenoceptor (β-AR) in the basolateral nucleus of amygdala (BLA) is important for reconsolidation of fear memory after retrieval. Rats were placed in chamber A and presented with a 30-s auditory cue (CS) . During the last 2s of the CS, rats were delivered with an electric shock to foot (US) . 24h post-conditioning, rats were placed in chamber B and given a single CS presentation to reactivate fear memory. The β-AR antagonist L-propranolol induced severe amnesia when infused into the BLA 0h post-retrieval of the memory, regardless of whether the reactivation was performed 1 day or 12 days post-conditioning. L-propranolol produced no amnesia if the memory was not activated or if given 6h post-reactivation. D-propranolol, which has an equipotent local-anesthetic activity but significantly lower β-blocking activity, induced no amnesia when given 0h post-reactivation. The present results indicate that β-AR in the BLA is essential for the reconsolidation of auditory fear memory after retrieval.NMDA receptor (NMDA-R) in the amygdala complex is critical for both long-term potentiation (LTP) and formation of fear memory. It is known that β-adrenoceptors (β-AR) in the amygdala is involved in regulating both LTP and memory consolidation. The present study examined the regulatory effect of β-adrenergic activation on NMDA-R mediated currents in pyramidal cells of basolateral nucleus of amygdala, using whole-cell patch-clamp recording technique. Bath application of the β-AR agonist isoproterenol enhanced NMDA-induced currents, and this facilitatory effect was blocked by co-administered propranolol, a β-adrenergic antagonist. This result suggests that β-AR in the BLA may modulate activation of NMDA receptors.