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Review
. 2012 Jan;62(1):3-12.
doi: 10.1016/j.neuropharm.2011.07.014. Epub 2011 Jul 27.

Stress and anxiety: structural plasticity and epigenetic regulation as a consequence of stress

Bruce S McEwen  1 , Lisa Eiland, Richard G Hunter, Melinda M Miller
Affiliations
Review

Stress and anxiety: structural plasticity and epigenetic regulation as a consequence of stress

Bruce S McEwen et al. Neuropharmacology. 2012 Jan.

Abstract

The brain is the central organ of stress and adaptation to stress because it perceives and determines what is threatening, as well as the behavioral and physiological responses to the stressor. The adult, as well as developing brain, possess a remarkable ability to show reversible structural and functional plasticity in response to stressful and other experiences, including neuronal replacement, dendritic remodeling, and synapse turnover. This is particularly evident in the hippocampus, where all three types of structural plasticity have been recognized and investigated, using a combination of morphological, molecular, pharmacological, electrophysiological and behavioral approaches. The amygdala and the prefrontal cortex, brain regions involved in anxiety and fear, mood, cognitive function and behavioral control, also show structural plasticity. Acute and chronic stress cause an imbalance of neural circuitry subserving cognition, decision making, anxiety and mood that can increase or decrease expression of those behaviors and behavioral states. In the short term, such as for increased fearful vigilance and anxiety in a threatening environment, these changes may be adaptive; but, if the danger passes and the behavioral state persists along with the changes in neural circuitry, such maladaptation may need intervention with a combination of pharmacological and behavioral therapies, as is the case for chronic or mood anxiety disorders. We shall review cellular and molecular mechanisms, as well as recent work on individual differences in anxiety-like behavior and also developmental influences that bias how the brain responds to stressors. Finally, we suggest that such an approach needs to be extended to other brain areas that are also involved in anxiety and mood. This article is part of a Special Issue entitled 'Anxiety and Depression'.

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Figures

Figure 1
Figure 1. Effect of chronic restraint stress on the number of apical and basal (upper and lower panel on left) dendritic branch points and total dendritic length (upper and lower panel on right) of CA3 pyramidal neurons from wild type and haploinsufficient BDNF (BDNFBl/6) mice
* * and *P < 0.01 and P < 0.05 respectively, compared with control wild types. One-way ANOVA, Tukey post hoc test. Bars represent means 1 SEM. From (Magarinos et al 2011).
Figure 2
Figure 2. Changes in dentate gyrus histone H3K9 trimethylation after acute immobilization stress as well as 7 and 21 day repeated immobilization stress
Acute stress induces a 2-fold increase in H3K9me3 levels. Adapted from (Hunter et al 2009b).
Figure 3
Figure 3. Duration of time spent in open arms of elevated plus maze 24 h after termination of CRS
There was a significant effect of rearing on the percent time spent in the open arms of the EPM. MS-CRS spent significantly less time in the open arms than all other groups. NMS rats spent 25.98 6 4.64%, NMS-CRS 24.44 6 4.05%, MS 22.38 6 4.58%, and MS-CRS 12.03 6 2.40%. Two-way ANOVA rearing effect F1,42 5 4.83, *P 5 0.03, n 5 11–14 for all groups. From Eiland and McEwen, 2011.
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