Understanding Stress

Characteristics of the Stressor, Part 2
by National Institute of Health

(Page 3 of 6)

Although researchers may be tempted to conclude that the ability to neutralize a stressor is the fundamental feature in predicting neurochemical and behavioral change, this conclusion may be premature. For instance, when stressed animals are permitted to fight with a member of their species, the effects ordinarily elicited by uncontrollable stressors may be mitigated, a phenomenon known as displacement. Nevertheless, displacement aggression may not eliminate the stressor and may in fact create additional stress. An important aspect of displacement behaviors, such as aggression, is that by offsetting the impact of stressors, the displacement behaviors may become reinforced. AOD use may serve, in part, as such a displacement behavior. Whether or not the displacement behaviors related to stressful events actually support both the initiation and maintenance of AOD abuse remains to be determined.

Not all neurochemical or physiological processes are differentially influenced by stressor controllability. The ability to respond rapidly to a stressful challenge may have greater adaptive value than the ability to assess controllability. Moreover, determining whether a given stressor is controllable may require sustained or repeated exposure, a luxury that may not be affordable. Thus, systems designed for immediate response (activation of the HPA axis or the immune system) ought to react comparably to both controllable and uncontrollable stressors. Conversely, systems that are uniquely involved in the appraisal of processive stressors might react differently to controllable than to uncontrollable stressors.

Studies in humans support the view that stressor controllability may be fundamental in determining the stress response, despite the fact that in a great number of instances, control is actually illusory. Rather than assessing stressor controllability, researchers may find it more profitable to consider the specific coping mechanisms that are available to the individual. Broadly speaking, coping can be subdivided into several subtypes, including emotion-focused coping (emotional expression, emotional containment, blame, avoidance, denial, and passivity); problem-focused coping; social support; cognitive restructuring; and problem-solving.

Researchers often assume that emotion-focused coping is a relatively ineffective strategy, whereas social buffering, problem-solving, and cognitive restructuring may be more efficacious. To some extent, this conclusion is based on findings that depressed patients, relative to control subjects, tend to favor emotion-focused coping and revert to a more problem-focused strategy with successful treatment. Although emotion-focused coping can be ineffective and even counterproductive, the effectiveness of a strategy may depend on the specific stressor regimen. A given strategy may be ineffective under one set of conditions but be highly effective under another. Ultimately, the abilities to maintain flexibility and be prepared to use different strategies may be the hallmark of effective coping.

Nerve Cell Communication and the Stress Response

Nerve cells communicate with one another through chemical messengers called neurotransmitters. The neurotransmitters discussed in this article interact extensively to perform a variety of regulatory activities. Serotonin affects a wide range of physiological functions, including appetite, sleep, and body temperature. Serotonin also influences emotional states, and its dysfunction has been implicated in both psychiatric and addictive disorders. Dopamine helps regulate goaldirected behaviors (including the reinforcing effects of alcohol and other drugs) as well as certain motor functions. Within the brain, norepinephrine plays a role in arousal and in the modulation of other neurotransmitter systems. When released into the bloodstream by the adrenal glands, norepinephrine functions as a stress-related hormone, preparing the body for "fight or flight" in response to threatening situations.

Chronicity and Predictability

Intuitively, one would suspect that the behavioral and neurochemical impact of an acute stressor would be exacerbated by repeated exposure to the stressor. However, some stressor-induced behavioral, neurochemical, and immunological disturbances in rats and mice may be mitigated by prolonged stressor exposure. For example, the decline of brain NE concentrations associated with acute stressor exposure may reverse following protracted or repeated exposure. Such adaptation appears to represent an active process, because NE levels in chronically stressed animals do not simply return to prestress levels but, instead, exceed basal values. Chronic stressors appear to promote a compensatory increase in the production of NE (or, in the case of DA, moderation of excessive utilization), leading to increased neurotransmitter concentrations.

Factors that prevent or limit neurochemical adaptation may be associated with behavioral or physiological disorders. For example, some of the behavioral and neurochemical changes associated with chronic predictable stressors are less apt to appear following chronic unpredictable stressors. Interestingly, a regimen of chronic mild stressors may result in an inability to experience pleasure (anhedonia) similar to that elicited by relatively intense stressors. Thus, even stressors that have modest effects when applied acutely may have pronounced behavioral repercussions when experienced on a chronic, unpredictable basis.

In humans, stressors are typically of a varied nature, are encountered on an intermittent and unpredictable basis, and may be experienced over protracted periods. As indicated earlier, many stressors have secondary effects (rumination, financial loss, or loss of social support), which are themselves stressful or limit coping abilities. A chronic, intermittent stressor regimen is less likely to lead to neurochemical adaptation and, hence, favor the development of pathology. When the chronic stressor regimen is not only unpredictable, but is also uncontrollable and associated with secondary stressors, the occurrence of behavioral disturbances might, perhaps, increase.

Two important caveats must be stressed with respect to the impact of chronic stressors. First, the compensatory neurotransmitter changes associated with repeated stressor exposure vary widely and occur in several brain regions. Not all of these variations necessarily progress at comparable rates or in all species of laboratory animals. Thus, the nature of the pathology associated with a chronic stressor regimen may depend on the specific neurochemical disturbances incurred. Second, the process of coping with chronic stressor exposure creates prolonged and intense demands on neurochemical systems, a condition termed "allostatic load." Sustained and excessive allostatic load may culminate in pathological outcomes. Evaluating the contribution of stressors to behavioral disturbances (alcoholism) in humans requires large-scale prospective studies assessing the impact of acute and chronic insults, the contribution of coping factors, and allostatic load associated with certain stressor regimens.

About the Author

NIH is the nation's medical research agency - making important medical discoveries that improve health and save lives. The National Institutes of Health (NIH), a part of the U.S. Department of Health and Human Services, is the primary Federal agency for conducting and supporting medical research.