Insular cortex and amygdala lesions induced after aversive training impair retention: effects of degree of training

These experiments examined the effects of N-methyl-D-aspartate (NMDA)-induced lesions of the amygdala and insular cortex induced 1 week after rats were trained on a footshock motivated escape task in a two-compartment runway. In the first experiment, male rats were given 10 training trials and, 1 week later, received microinjections of a buffer solution or NMDA into either the insular cortex (IC) or the amygdala (AM). In an inhibitory avoidance retention test 1 week after the microinjections, the retention latencies (i.e., latencies to enter the compartment where shock had been delivered) of both the AM- and "IC-lesioned" groups were significantly lower than those of the buffer-injected groups. Additionally, in comparison with the buffer controls, rats in the two lesioned groups made significantly more crossings between the two compartments during the retention test. In a second experiment, male rats were given 1, 10, or 20 escape training trials 1 week before receiving either sham or NMDA lesions in the IC. The retention test was given 1 week after microinjection. Those sham or lesioned animals that were given only one training trial did not demonstrate retention. Both lesioned groups given 10 or 20 training trials were significantly disrupted on both the step-through latencies, and the number of crossings between the two compartments. The retention-impairing effects of NMDA-induced lesions were slightly attenuated in the group given 20 escape training trials. The findings provide additional evidence that the AM and the IC are involved in regulating the long-term retention of aversively motivated training.