Abstract

Studies have shown that, depending on its severity and context, stress can affect neural plasticity. Most related studies focused on synaptic plasticity and long-term potentiation (LTP) of principle cells. However, evidence suggests that following high-frequency stimulation, which induces LTP in principal cells, modifications also take place at the level of complex interactions with interneurons within the dentate gyrus, that is, at the local circuit level. So far, the possible effects of stress on local circuit activity and plasticity were not studied. Therefore, we set out to examine the possible alterations in local circuit activity and plasticity following exposure to stress. Local circuit activity and plasticity were measured by using frequency dependant inhibition (FDI) and commissural modulation protocols following exposure to a 15 minute-forced swim trial. Exposure to stress did not alter FDI. The application of theta-burst stimulation (TBS) reduced FDI in both control and stressed rats, but this type of plasticity was greater in stressed rats. Commissural-induced inhibition was significantly higher in stressed rats both before and after applying theta-burst stimulation. These findings indicate that the exposure to acute stress affects aspects of local circuit activity and plasticity in the dentate gyrus. It is possible that these alterations underlie some of the behavioral consequences of the stress experience.

Highlights

  • Stress is defined as any condition that seriously disrupts physiological and psychological homeostasis ranging from anxiety to posttraumatic stress disorder [1], and affects cognitive functions both in animal models and in humans [2,3,4]

  • We have examined the effects of behavioral stress on local circuit activity and plasticity in the dentate gyrus (DG)

  • We report that when using frequency dependant inhibition (FDI) [26], this form of local circuit activity was reduced following the application of theta-burst stimulation (TBS) in both control and stressed rats

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Summary

Introduction

Stress is defined as any condition that seriously disrupts physiological and psychological homeostasis ranging from anxiety to posttraumatic stress disorder [1], and affects cognitive functions both in animal models and in humans [2,3,4]. Long-term potentiation (LTP) of synaptic transmission in the hippocampus is the most studied neurophysiological model for learning and memory processes in the mammalian nervous system. Depending on the type of stress and the procedures used, stress has been shown to have different effects on different measures of synaptic plasticity. There is a general agreement that LTP in area CA1 of the hippocampus is impaired following stress [4, 14,15,16,17,18]. Some studies have shown that stress impairs LTP in the dentate gyrus (DG) of the hippocampus [16, 19, 20], while others reported intact LTP in the DG following stress [14, 21]. DG LTP is considered to be less sensitive to stress compared to LTP in CA1 [22]

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