Effects of Novel versus Repeated Mild Stressful Experiences on Long‐Term Potentiation Induced Simultaneously in the Amygdala and Hippocampus in Freely Behaving Rats

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stress, long‐term potentiation, amygdala, hippocampus

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A variety of findings suggest that the amygdala and the hippocampus represent two rather different but interacting memory systems. Of significant interest is their interaction during stress, which may help explain the controversial and sometimes confusing effects of stress on memory, with stress sometimes enhancing, impairing, or having no effect on memory or long‐term potentiation (LTP).1, 2 LTP is one type of synaptic plasticity that has been implicated in some forms of hippocampus‐ and amygdala‐dependent memory processing. Consistent with a dynamic interactive view of amygdala and hippocampus function, the present series of experiments examined their possible simultaneous activation by the direct projections from the entorhinal cortex (EC). In addition, we studied the effects of novel vs. familiar stress on immobility and simultaneously induced LTP in the amygdala and hippocampus. Stimulation of EC evoked in the amygdaloid basal nucleus (B) and in the dentate gyrus (DG), field potentials consisting of negative‐positive and positive‐negative waveforms, respectively. Theta burst stimulation of the EC induced late‐phase LTP simultaneously in B and in DG. However, the mechanisms involved differ between the two areas as the NMDA receptor antagonist CPP blocked LTP in the DG but not in B. In light of the known functional interactions between the basolateral amygdala complex (comprised of lateral, basal, and accessory basal nuclei) and the DG, the results suggest a coordinating role for the EC by simultaneously modulating activity and plasticity in these structures. Furthermore, the ability of both areas to sustain late‐phase LTP supports a role for both in memory formation, albeit of different types and mechanisms.

It is know that certain types of stress suppress hippocampal LTP as well as hippocampal‐dependent memory processes. However, the effects of stress on the amygdala are less known. Since the amygdala is recognized to mediate stress responses, stress may have opposite effects on amygdala activity and plasticity. In a preliminary set of experiments, we compared the effects of stress on simultaneously induced LTP in B and DG. A mild stress was induced by placing rats on a platform in a circular pool in a brightly lightened room. Stress consisted of either a single exposure (‘novel stress’) or two exposures on two consecutive days (‘repeated stress’). Immobility was higher in the ‘repeated stress’ rats than in the ‘novel stress’ group. Preliminary results suggest that novel stress facilitates both early‐ and late‐phase LTP in B but has little effect on LTP in DG. In contrast, repeated stress inhibits late‐LTP in B as well as both early‐ and late‐LTP in DG. Collectively, these results suggest novel stress to be a learning‐supporting situation, whereas repeated stress may induce a depressive‐like status in which learning and memory are hampered. Furthermore, the results point to the possibility that the relative involvement of the amygdala and hippocampus in memory formation differs depending on the emotional context of the experience.

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Annals of the New York Academy of Sciences, v. 985, issue 1, p. 556-557