Literature DB >> 21763760

Chronic stress modulates neural and cardiovascular responses during reversal learning.

H Ohira1, M Matsunaga, K Kimura, H Murakami, T Osumi, T Isowa, S Fukuyama, J Shinoda, J Yamada.   

Abstract

Animal studies have revealed that chronic stress shifts cognitive strategies from the flexible goal-directed action to the simple and rigid habit action. In addition, stress-induced atrophy in the prefrontal cortex and dorsomedial striatum which are involved in the goal-directed action and hypertrophy of the dorsolateral striatum which is critical for the habit action were parallel with the effects of chronic stress on behaviors. The present study tested whether these previous findings in animal studies are compatible in humans by analyzing effects of chronic stress on neural and cardiovascular responses, which are likely important for performing appropriate actions. Twenty healthy men exposed to low or high chronic job stress performed a stochastic reversal learning task, which required cognitive flexibility and the goal-directed action. Regional cerebral blood flow was evaluated during the task using (15)O-water positron emission tomography, and cardiovascular parameters such as blood pressure and heart rate were also measured. During the reversal learning task, whereas participants with low chronic job stress exhibited activity in the anterior caudate, as well as orbitofrontal cortex, ventrolateral prefrontal cortex, insula, and midbrain, which might be related to the goal-directed action, participants with high chronic job stress exhibited no activity in such brain regions. Furthermore, participants with high chronic job stress exhibited less reactivity in diastolic blood pressure, which might be mediated by anterior cingulate cortical activity. These findings, in line with previous studies, suggested that chronic job stress correlates with less activity in brain regions related to the goal-directed action, and insensitive physiological responses in humans.
Copyright © 2011 IBRO. Published by Elsevier Ltd. All rights reserved.

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Year:  2011        PMID: 21763760     DOI: 10.1016/j.neuroscience.2011.07.014

Source DB:  PubMed          Journal:  Neuroscience        ISSN: 0306-4522            Impact factor:   3.590


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