The basolateral amygdala is a cofactor in memory enhancement produced by intrahippocampal glutamate injections
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In the present experiments, the modulatory influence of the basolateral amygdala on hippocampal-dependent memory processes was examined. Adult male Long-Evans rats were trained in a dally session in a win-shift radial maze task to obtain food from four randomly selected maze arms. After a delay period, they were returned to the maze with all the arms accessible and allowed to obtain four pellets from those arms that were not previously visited. Following criterion training with 5- and 15-min delay periods, the rats were given a drug test in which they received a posttraining intracerebral drug treatment immediately following the first four food- rewarded choices. In Experiment 1, the treatment consisted of an intrahippocampal or intra-amygdala injection (0.5 l) of either a 2% solution of the local anesthetic lidocaine or saline. Four hours after injection, the rats were returned to the maze for a retention test. Posttraining intrahippocampal, but not intra-amygdala, injections of lidocaine impaired retention test choice accuracy. In Experiment 2, the rats unilaterally cannulated in two brain regions (the hippocampus and the basolateral amygdala) received posttraining intrahippocampal injections of glutamate or saline and concurrent intra-amygdala injections of lidocaine or saline. Intrahippocampal injection of glutamate (2.0 g/0.5 l) enhanced memory in the win-shift task when an 18-h delay was used. Concurrent posttraining intra-amygdala injections of lidocaine blocked the memory- enhancing effects of intrahippocampal glutamate administration. The findings suggest that, although a functional basolateral amygdala is not essential for normal memory in a hippocampal-dependent win-shift radial maze task, the basolateral amygdala is a necessary cofactor in the memory-enhancing effects of posttraining intrahippocampal injections of glutamate.