Abstract

It has been known that the amygadala is the neural substrate for conditioned fear as well as unconditioned fear. Among the substructures of amygdala, the basolateral nucleus where CS and US inputs converge and LTP occurs, contains high densities of NMDA receptors and so seems to have a critical role in synaptiplasticity. NMDA antagonist, AP5 prevent induction of Long-term potentiation, but not expression of LTP. LTP is an activity dependent enhancement of synaptic efficacy and is regarded the psysiological mechanisms that might underlie learning and memory. So this experiment was done to investigate what effect AP5 injection to the basolateral amygdala on the acquisition and expression of the fear conditioning, using the fear potentiated Startle paradigm. Animals were allocated to AP5-AP5, AP5-saline, saline-AP5, saline-saline groups. AP5 or saline was injected just before conditioning and testing. The re sult is that AP5-AP5, AP5-saline group didn`t show the potentiated startle, comparative to the saline-AP5, saline-saline group, and AP5-AP5 group is not significantly different from AP5-saline. So we conclude that AP5 blocked the acquisition but not expression of conditio-ned fear-potentiated startle and convince that the blocking is not due to state-dependent retrieval failure.