Abstract

Stress is a potent modulator of the mammalian brain. The highly conserved stress hormone response influences many brain regions, particularly the hippocampus, a region important for memory function. The effect of acute stress on the unique population of adult neural stem/progenitor cells (NPCs) that resides in the adult hippocampus is unclear. We found that acute stress increased hippocampal cell proliferation and astrocytic fibroblast growth factor 2 (FGF2) expression. The effect of acute stress occurred independent of basolateral amygdala neural input and was mimicked by treating isolated NPCs with conditioned media from corticosterone-treated primary astrocytes. Neutralization of FGF2 revealed that astrocyte-secreted FGF2 mediated stress-hormone-induced NPC proliferation. 2 weeks, but not 2 days, after acute stress, rats also showed enhanced fear extinction memory coincident with enhanced activation of newborn neurons. Our findings suggest a beneficial role for brief stress on the hippocampus and improve understanding of the adaptive capacity of the brain. DOI:http://dx.doi.org/10.7554/eLife.00362.001.

Highlights

  • Stress is a powerful and essential mediator of mammalian behavior

  • We show that astrocyte-secreted fibroblast growth factor 2 (FGF2) is necessary for CORT-induced enhancement in neural stem/ progenitor cells (NPCs) proliferation in vitro. 2 weeks after acute stress, when newborn neurons are first becoming functional, we find enhancement in hippocampus-dependent memory accompanied by enhanced activation of newborn neurons

  • We investigated whether blocking FGF2 function could prevent acute stress-induced enhancement of NPC proliferation using a neutralizing antibody against FGF2

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Summary

Introduction

Proper response to a perceived stressor facilitates survival at the individual level and species propagation at the population level Despite this necessity, stress responses can become maladaptive. One model of stress effects on the brain, an inverted U function, explains the variable consequences of acute stress for brain health (Lupien and McEwen, 1997). In this model, while severe or prolonged stressors are detrimental, brief or moderate stressors enhance neural function. Behavioral studies focusing on the memory functions of the hippocampus have demonstrated such a relationship in rodents, where moderate stress enhances memory performance yet more severe stress impairs it (Conrad et al, 1999)

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