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ANSWER:
Normally, activity of the HPA axis is regulated by a feedback loop involving the hippocampus. As the text analogizes, the hippocampus works like a rev limiter in an automobile engine that prevents the driver from going over a certain speed. The hippocampus contains large numbers of receptors for cortisol and other stress hormones. When the hippocampus detects high levels of these hormones, it signals the hypothalamus, which in turn tells the adrenal glands to reduce the release of cortisol, and arousal in response to perceived stressors dissipates. Consistently elevated levels of cortisol due to chronic stress can overwhelm the hippocampuss feedback loop, leading instead to the continuous release of cortisol and constant arousal.
Students may describe some of the following adverse health effects:
Long-term exposure to cortisol can produce a number of harmful effects, including the death of neurons. When rats received daily injections of the rat equivalent of cortisol, neural death began to occur in just a few weeks. Identical amounts of neural death occurred if the rats were stressed daily instead of receiving the injections, suggesting that the action of cortisol is responsible for most of the neural damage observed to result from stress. Studies in humans who have a medical condition (Cushings disease) that results in unusually high cortisol levels suggest that cortisol abnormalities might contribute to reduced hippocampus volume, memory problems, abnormal sleep patterns, and depression. Not only can high levels of cortisol damage neurons, but these same levels appear to inhibit the neurogenesis, or birth of new neurons, that might help to offset the damage.
Continued stress can damage the hippocampus further. The stressed lower status baboons mentioned in the text, who had been placed in cages with higher status baboons by Kenyan farmers to protect their crops, experienced neural death, particularly in the hippocampus, in addition to their other medical problems. People with posttraumatic stress disorder also show evidence of having a smaller than average hippocampus. Having a smaller than average hippocampus might make a person exposed to trauma more vulnerable to the development of PTSD, or elevated levels of cortisol could reduce the size of the hippocampus, or both.
The role of the hippocampus as the rev limiter of the HPA axis might be the bridge between extreme stress and depression. Many cases of depression are preceded by unusually stressful events. Consistently elevated levels of cortisol due to stress can overwhelm the hippocampuss feedback loop, leading instead to the continuous release of cortisol and constant arousal. Without the regulation of cortisol usually provided by the hippocampus acting as a rev limiter, a person can begin to experience depression. Patients who are treated with cortisol and similar stress hormones for medical conditions such as rheumatoid arthritis are often troubled by deep depression, reinforcing the role of excess cortisol in depressed mood.
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