The two principal kinds of emotional behavior influenced by endocrine glands are those related to stress and those related to gender-specific sexual behavior. Gender-specific behaviors are not only those behavioral patterns involved in mating and care of the young, but also acts such as intermale aggression not directly involved in reproduction of the species. Certain of the gonadotropins are necessary to organize the development of the neuronal circuits that underlie these behaviors.
Terms used to classify emotions generally include happiness, love, grief, guilt, and joy. However, most of these are impossible to define with sufficient operational rigor to permit scientific study, especially when animal models are used to unravel the neural and endocrine contributions to the emotional state and accompanying behavior. This is because these categories of emotion have not been constructed and refined from empirical observation. Rather, they are words taken from everyday language that describe either the speaker's introspective state or the internal state of another individual inferred from that individual's behavior. Therefore, the contribution of the neuroendocrine systems to many emotional states commonly described in everyday terms is not known. However, the relationship between stress and the neuroendocrine system is well established, and this relationship may be extended to the states of fear and anxiety.
Fear may be usefully regarded as a response to a specific stimulus present in the environment, whereas anxiety is an anticipatory response to a possible threatening event. Fear, then, is generally a shorter-lived state, whereas anxiety may be chronic and generalize to the degree to which it is not bound to a specific stimulus. However, both of these states produce similar endocrine responses. The simplest of these responses involves discharge from the sympathetic neurons located in the spinal cord. The axons of the sympathetic neurons terminate on visceral organs, including arteries. Their activity during periods of stress increases blood pressure, heart and respiratory rates, and the release of liver glucose stores, while gastrointestinal motility is decreased. In addition, sympathetic activation of the adrenal medulla increases the release of adrenalin and noradrena-lin into the bloodstream.
The adrenal cortex also is involved in response to either acute (fear) or chronic (anxiety) stress. However, the adrenal cortex is not directly activated by the sympathetic nervous system. As noted earlier, the adrenal cortex is activated by adrenocorticotropic hormone (ACTH). ACTH is released from the adenohypophysis (anterior pituitary) and stimulates the adrenal cortex to release glucocorticoids (cortisol, cortisone, and corticosterone). The glucocorticoids increase cardiac and vascular muscle tone, enhance the release of nutrients into the blood, decrease inflammation, and inhibit protein synthesis. The release of ACTH by the anterior pituitary is controlled by the hypothalamic hormone, corticotropin-releasing factor (CRF). CRF is manufactured by neurons in the paraventricular nucleus of the hypothalamus and is transported down the axons of these neurons and released into the portal circulation of the ade-nohypophysis where it stimulates release of ACTH. The paraventricular nucleus is strongly influenced by structures in the limbic system, such as the amygdala, that are involved in modulation of fear responses. The secretion of glucocorticoids by the adrenal cortex is closely linked to parts of the brain involved in elaboration of fear states and intensification of behaviors that accompany them.
Activation of both the sympathetic-adrenal medullary response and the hypothalamic-pituitary-adrenal cortical response are obviously adaptive in the face of immediate, comparatively short-term threat. These responses help the organism to fight or flee. However, as described by Selye, continual activation of these systems by chronic stress can lead to serious consequences for health. Selye referred to the changes produced by long-term stress as the general adaptation syndrome (GAS) and divided it into three stages. The first stage is the alarm reaction during which the body significantly increases the production and release of the stress hormones. This first stage lasts only a few hours, but the second stage, resistance, may continue for days or weeks. During this stage, blood levels of adrenalin, noradrenalin, and the glucocorticoids remain high. The final stage is exhaustion when the body can no longer respond to the stress.
GAS may be brought about by any stressful situation, including chronic physical stress (e.g., from exposure to extreme cold or in times of real physical danger), but it also may occur as a result of continual psychological stress. As originally described by Selye, the physical correlates of GAS include enlarged adrenal glands, with a marked increased in size of the adrenal cortex as its cells respond to the actions of ACTH and attempt to produce ever larger quantities of the glucocorticoids, as well as a shrunken thymus, weight loss, and gastric ulcers. Gastric ulcers are caused by chronic decrease in blood flow to the gut. Substantial rates of blood flow are necessary for maintenance of the mucosal lining that protects the stomach from the digestive acids. As a consequence of chronic activation of the body's stress response, the gut's blood flow is so decreased that its mucosal lining deteriorates, and the stomach's hydrochloric acid produces ulcers.
The cause of the shrinkage of the thymus noted in GAS is not known. The thymus is responsible for producing many of the lymphocytes (key cells in the immunologic defense of the body from infection), and chronic stress decreases the ability of the immune system to respond. The mechanism for stress-induced reduction in immune responsiveness is known and involves the increased amounts of circulating glucocorticoids present during stress.
Enhanced levels of glucocorticoids decrease protein synthesis. As a short-term part of a response to threat this is useful because it conserves metabolic energy. However, the decreased protein synthesis extends to those proteins that form the receptors on cells that recognize foreign elements in the blood. These receptors constitute antibodies, and the cells are the white blood cells (leukocytes), including the lymphocytes. During stress, production of both the antibody receptors and the cells that carry these receptors decreases. Prolonged periods of stress results in immunosup-pression and increased susceptibility to infectious disease and the development of cancer.
Abnormally high levels of the glucocorticoid cortisol also have been found in 40-60% of depressed patients and is known to be caused by enhanced secretion of CRF by the hypothalamus. The hypersecretion of CRF by the hypothalamus is probably a specific effect of the general dysfunction of the ascending aminergic neurotransmitter systems (dopamine, norepinephrine, and serotonin) thought to be the biological cause of depression.
The overall effect of activation of the neuroendocrine systems involved in response to stress is to produce a state of enhanced readiness for physical action without neces sarily activating specific neural circuits that produce directed behaviors. Although such activation may be beneficial for survival in the face of real threat, prolonged activation of these systems is detrimental to health.
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