Norepinephrine and CRH can produce other adaptive responses to stressors when they act locally on brain nerve cells as neurotrans-mitters. For example, their actions on the CNS result in a general state
of arousal and aggressiveness. They also can inhibit behaviors such as growth, reproduction, ovulation, sexual activity, and eating, which is necessary when the body’s internal homeostatic balance has been disrupted. Considered collectively, these effects illustrate the integration between the nervous, endocrine, and immune systems.
Besides norepinephrine and CRH, at least five other chemicals involved in transmission of nerve impulses in the brain neurochemicals may play an integrating role in coordinating the body’s responses to stressors. Serotonin, for example, directly affects ACTH and prolactin secretion. Dopamine a catecholamine precursor of norepinephrine release in the brain increases with exposure to various stressors. The neurotransmitter GABA gamma-aminobutyric acid and endogenous opioids inhibit the function of the HPA axis. Also, acetylcholine excites the release of CRH. These effects not only emphasize the complexity of the body’s response to stressors, but also remind us that the SAM and HPA hormonal axes see figureare not the only pathways available.
Scientific observations also provide evidence for interactions between the nervous system and the immune system. These include the following:
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Underwater welders experience extreme environments as part of their daily work. © Tom McCarthy/Unicorn Stock Photos
Animals exposed to stressors have altered immune status.
Electrical stimulation of specific brain regions alters immune function.
Changes in hormone and physiological exercise activities in brain cells are correlated with activation of the immune system.
In addition to the activities in the SAM and HPA hormonal axes, the secretion of other hormones changes when stressors are encountered. These hormones can be classified as either anabolic enhanced metabolism and tissue construction or catabolic decreased metabolism and tissue destruction. The former include insulin, testosterone, and estrogen; the latter include growth hormone, prolactin the pregnancy hormone important for lactation and thyroxine, in addition to epinephrine, norepinephrine, and cortisol. Interestingly, during a period of increased exposure to stressors, secretion of the catabolic hormones increases and the levels of the anabolic hormones in blood decrease. The end result, during stressful experiences, is a mobilization of energy reserves, as exhibited by growth hormone, prolactin, and thyroxine, which mobilize free fatty acids from adipose tissue. The poststressor outcome when secretion of anabolic hormones increases and production of catabolic hormones decreases builds depleted energy stores and replaces lost body tissue; for example, insulin promotes the storage of glucose and fats, and testosterone promotes protein synthesis.
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