Abstract

Recent findings on stress induced structural plasticity in rodents have identified important differences between the hippocampus and amygdala. The same chronic immobilization stress (CIS, 2h/day) causes growth of dendrites and spines in the basolateral amygdala (BLA), but dendritic atrophy in hippocampal area CA3. CIS induced morphological changes also differ in their temporal longevity- BLA hypertrophy, unlike CA3 atrophy, persists even after 21 days of stress-free recovery. Furthermore, a single session of acute immobilization stress (AIS, 2h) leads to a significant increase in spine density 10 days, but not 1 day, later in the BLA. However, little is known about the molecular correlates of the differential effects of chronic and acute stress. Because BDNF is known to be a key regulator of dendritic architecture and spines, we investigated if the levels of BDNF expression reflect the divergent effects of stress on the hippocampus and amygdala. CIS reduces BDNF in area CA3, while it increases it in the BLA of male Wistar rats. CIS-induced increase in BDNF expression lasts for at least 21 days after the end of CIS in the BLA. But CIS-induced decrease in area CA3 BDNF levels, reverses to normal levels within the same period. Finally, BDNF is up regulated in the BLA 1 day after AIS and this increase persists even 10 days later. In contrast, AIS fails to elicit any significant change in area CA3 at either time points. Together, these findings demonstrate that both acute and chronic stress trigger opposite effects on BDNF levels in the BLA versus area CA3, and these divergent changes also follow distinct temporal profiles. These results point to a role for BDNF in stress-induced structural plasticity across both hippocampus and amygdala, two brain areas that have also been implicated in the cognitive and affective symptoms of stress-related psychiatric disorders.

Highlights

  • Accumulating evidence indicates that the same behavioral stress, such as 10 days of chronic immobilization stress (2 hours/ day), can elicit contrasting patterns of structural plasticity in the rat hippocampus and amygdala simultaneously [1,2,3]

  • We report that the same chronic immobilization stress (CIS) has strikingly opposite effects on brain-derived neurotrophic factor (BDNF) expression one day after the end of CIS – it reduces BDNF in area CA3, while it increases BDNF in the basolateral amygdala (BLA)

  • In light of earlier reports on the unique temporal features of structural plasticity elicited in the amygdala by both chronic and acute stress, we tested whether changes in BDNF levels exhibit distinct patterns across time in the two areas

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Summary

Introduction

Accumulating evidence indicates that the same behavioral stress, such as 10 days of chronic immobilization stress (2 hours/ day), can elicit contrasting patterns of structural plasticity in the rat hippocampus and amygdala simultaneously [1,2,3]. A much shorter duration of the same stress, such as a single 2 h episode of immobilization, that fails to affect spine density or dendritic arborization one day later, leads to a significant increase in spine density ten days later [8]. Together, these studies have helped identify novel features of stress-induced plasticity in the amygdala that are quite distinct from those observed in the hippocampus

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