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Comprehensive PhysiologySee 2016's top cited articles

Some stress, of course, can be beneficial. The pressure it exerts can be an incentive to accomplish necessary goals. Often, however, stress reaches chronic, harmful levels, and deleterious consequences follow, from compromised immune function to weight gain to developmental impairment (2). The intensity of the stress response is governed largely by glucocorticoids, the primary molecules involved in the stress response. Stress can be ephemeral and beneficial, or it can be long-lasting and harmful, causing suffocation, depression, and paralysis (3). Proper stress management takes on great importance given the wide range of bodily systems impacted by stress hormones.

James B. Young, Lewis Landsberg

Several studies have recently shown that basal and stress-induced secretion of corticosterone may enhance vulnerability to drugs of abuse. In this report, we studied the effects of metyrapone, an inhibitor of the synthesis of corticosterone, on cocaine-induced locomotion and on the relapse of cocaine self-administration. Locomotor response to cocaine was studied because psychomotor effects of drugs have been shown to be related to their reinforcing properties. Self-administration was studied in the relapse phase since blockade of relapse is central to the therapy of addiction. Before these behavioral tests, rats in different experimental groups were injected subcutaneously with either metyrapone (100 mg/kg) or vehicle, twice a day for 8 days. Metyrapone treatment reduced cocaine-induced locomotor activity and relapse of cocaine self-administration, without inducing a nonspecific disruption of motor or food-directed behaviors. Under these experimental conditions, the metyrapone treatment totally blocked stress-induced corticosterone secretion but did not modify basal corticosterone levels. These results confirm the involvement of glucococorticoids in the pathophysiological mechanisms underlying vulnerability to drug abuse, and may have implications for the development of new therapeutic strategies of drug addiction.

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AB - Several studies have recently shown that basal and stress-induced secretion of corticosterone may enhance vulnerability to drugs of abuse. In this report, we studied the effects of metyrapone, an inhibitor of the synthesis of corticosterone, on cocaine-induced locomotion and on the relapse of cocaine self-administration. Locomotor response to cocaine was studied because psychomotor effects of drugs have been shown to be related to their reinforcing properties. Self-administration was studied in the relapse phase since blockade of relapse is central to the therapy of addiction. Before these behavioral tests, rats in different experimental groups were injected subcutaneously with either metyrapone (100 mg/kg) or vehicle, twice a day for 8 days. Metyrapone treatment reduced cocaine-induced locomotor activity and relapse of cocaine self-administration, without inducing a nonspecific disruption of motor or food-directed behaviors. Under these experimental conditions, the metyrapone treatment totally blocked stress-induced corticosterone secretion but did not modify basal corticosterone levels. These results confirm the involvement of glucococorticoids in the pathophysiological mechanisms underlying vulnerability to drug abuse, and may have implications for the development of new therapeutic strategies of drug addiction.

Schematic representation of innervation of adrenal medulla. The various neuronal types that comprise the splanchnic nerve innervating the adrenal medulla. These include: afferent fibers of sensory nerves in dorsal root ganglion; postganglionic sympathetic nerves in paraspinal and suprarenal sympathetic ganglia; preganglionic sympathetic nerves innervating either epinephrine ()—or norepinephrine ()—containing chromaffin cells or medullary ganglion cells (GC); and fibers originating from ganglion cells traveling retrograde in splanchnic nerve to an unknown destination. refers to the intermediolateral column of the spinal cord from which the preganglionic sympathetic fibers arise.

Lock and key binding illustrated with the molecule adrenaline (right)

by John Wiley & Sons, Inc., or related companies. All rights reserved.

N2 - Several studies have recently shown that basal and stress-induced secretion of corticosterone may enhance vulnerability to drugs of abuse. In this report, we studied the effects of metyrapone, an inhibitor of the synthesis of corticosterone, on cocaine-induced locomotion and on the relapse of cocaine self-administration. Locomotor response to cocaine was studied because psychomotor effects of drugs have been shown to be related to their reinforcing properties. Self-administration was studied in the relapse phase since blockade of relapse is central to the therapy of addiction. Before these behavioral tests, rats in different experimental groups were injected subcutaneously with either metyrapone (100 mg/kg) or vehicle, twice a day for 8 days. Metyrapone treatment reduced cocaine-induced locomotor activity and relapse of cocaine self-administration, without inducing a nonspecific disruption of motor or food-directed behaviors. Under these experimental conditions, the metyrapone treatment totally blocked stress-induced corticosterone secretion but did not modify basal corticosterone levels. These results confirm the involvement of glucococorticoids in the pathophysiological mechanisms underlying vulnerability to drug abuse, and may have implications for the development of new therapeutic strategies of drug addiction.

Schematic representation of innervation of adrenal medulla. The various neuronal types that comprise the splanchnic nerve innervating the adrenal medulla. These include: afferent fibers of sensory nerves in dorsal root ganglion; postganglionic sympathetic nerves in paraspinal and suprarenal sympathetic ganglia; preganglionic sympathetic nerves innervating either epinephrine ()—or norepinephrine ()—containing chromaffin cells or medullary ganglion cells (GC); and fibers originating from ganglion cells traveling retrograde in splanchnic nerve to an unknown destination. refers to the intermediolateral column of the spinal cord from which the preganglionic sympathetic fibers arise.

A paper just out in the journal  has effectively refuted the claims of the Behe and Snoke paper (4)
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Stephen Meyer also argues on this line.

Finally, cortisol participates in an inhibitory feedback loop by blocking the secretion of corticotripin-releasing hormone, preventing the HPA axis interactions central to glucocorticoid secretion. Many in the scientific community speculate that chronic levels of high stress disrupt the delicate feedback balance, resulting in the failure of feedback inhibition to operate and the continued release of cortisol (15).

[I corrected a few typos -- Nick]

A role for cortisol in memory has also been demonstrated. The hippocampus, the region of the brain where memories are processed and stored, contains many cortisol receptors. While normal cortisol levels have no adverse effects on the hippocampus, excess cortisol overwhelms the hippocampus and actually causes atrophy. Studies of the elderly have indicated that those with elevated cortisol levels display significant memory loss resulting from hippocampus damage, but the exact age range at risk is unclear. There is a reprieve, however, for the chronically stressed: the damage incurred is usually reversible (14).

DANS is an institute of KNAW and NWO

Cortisol’s weakening effects on the immune response have also been well documented. T-lymphocyte cells are an essential component of cell-mediated immunity. T-cells respond to cytokine molecules called interleukins via a signaling pathway. Cortisol blocks T-cells from proliferating by preventing some T-cells from recognizing interleukin signals. It also stifles inflammation due to inhibition of histamine secretion (13). Cortisol’s ability to prevent the promulgation of the immune response can render individuals suffering from chronic stress highly vulnerable to infection.

Cited sample types include cell lysate, urine and whole blood.

Cortisol’s role in ion regulation, particularly regarding sodium and potassium, has also been widely studied. Cortisol prevents cells from losing sodium and accelerates the rate of potassium excretion. This helps regulates bodily pH, bringing it back into equilibrium after a destabilizing event. Cortisol’s ability to regulate the action of cellular sodium-potassium pumps has even led to speculation that it originally evolved as a sodium transporter (12).

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