Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pathological consequences of stress-induced activation of the hypothalamic-pituitary-adrenal (HPA) axis may be related to the duration rather than to the intensity of HPA axis activation after exposure to the stressor. Consequently a fine analysis of post-stress events is of importance. The present experiments were designed to study the importance of three key factors in HPA recovery: intensity of the stressor (experiment 1), duration of exposure to the stressor (experiment 2) and previous experience of the animals with the situation (experiments 3 and 4). In experiment 1, analysis of both the response to the stressor and the poststress period showed that the stronger the stressor, the greater the area under the curve of HPA activation. In experiment 2, different groups of rats were exposed to different periods of immobilization (IMO) (20 min, 1 h and 2 h) and sampled before, during and after exposure to IMO. The speed of recovery of plasma corticotropin (ACTH) levels was not related to the duration of exposure to the stressor. In experiments 3 and 4, the influence of previous experience with the stressor was studied in rats daily exposed to 20 min IMO or daily injected with hypertonic saline (HS) for 8 days and sampled on days 1, 2, 5 and 8. Whereas a significant decline in plasma ACTH levels was not observed immediately after IMO until day 8, a single previous exposure to IMO was enough to enhance recovery 90 min after the end of exposure to IMO. Corticosterone levels were related to the number of previous experiences with the stressor only in the post-IMO period. In response to a novel stressor (forced swimming), chronic IMO rats showed a slightly impaired recovery as compared to stress-naive rats, suggesting that enhanced recovery of the HPA axis was specific for the homotypic stressor. After daily HS injections, a pattern similar to that after IMO was observed, the delayed, but not the early response of the HPA axis being reduced as a function of the number of previous experiences with the situation. Taken together, the present results suggest that the speed of recovery of the HPA axis after its activation by stressors is sensitive to the intensity of the stressors but not to their duration, and that adaptation to a repeated stressor is more apparent during the delayed HPA response.
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PMID:Recovery of the hypothalamic-pituitary-adrenal response to stress. Effect of stress intensity, stress duration and previous stress exposure. 1097 Nov 46

Treatment with methamphetamine (MA) on postnatal days P11-20 induces adult spatial learning and memory deficits without affecting monoamine levels in various brain regions. In this study, we examined the pituitary and adrenal response of animals administered MA four times daily on P11, P11-15, or from P11 to P20. Corticosterone (CORT) and adrenocorticotropin hormone (ACTH) levels were assessed over a 1-hour period following MA exposure. On P11, MA produced marked elevations of both CORT and ACTH; this is during the stress hyporesponsive period (SHRP). On P15 and P20, the maximal effect of MA on CORT titers was observed at 30 min, with lower, but still significantly increased, levels at 60 min compared to controls. Males receiving MA on P15 had higher levels of ACTH than did control males, while no differences were noted among females. On P20, MA treatment resulted in higher levels of ACTH relative to vehicle-injected controls, but levels were not different from controls that were only weighed at each drug administration. MA treatment inhibited body, but not brain weight gain, resulting in hippocampal weights that were heavier in the MA-treated animals when expressed as a percent of body weight. The elevations of adrenal steroids by MA, during late phases of hippocampal neurogenesis, may contribute to neuronal alterations that are later manifested in deficits of learning and memory.
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PMID:Preweaning treatment with methamphetamine induces increases in both corticosterone and ACTH in rats. 1110 68

Previously we have shown that atrial natriuretic peptide (ANP) has anxiolytic-like properties after intraperitoneal, intracerebroventricular and intraamygdala infusion in rats. Since C-type natriuretic peptide (CNP) exerts endocrine and behavioral effects opposing those of ANP, we characterized the behavioral properties of CNP after icv infusion in rats by their performance in the elevated plus maze with and without the corticotropin-releasing hormone (CRH) antagonist alpha-helical-CRH (alpha-CRH). Low CNP doses of 0.05 microg icv or 0.1 microg icv did not significantly influence the behavior of rats in the plus maze. At higher doses (0.5 microg, 2 microg, 5 microg icv) CNP had distinct anxiogenic properties. Our hypothesis that corticotropin-releasing hormone (CRH) is involved, which elicits anxiety-like behavior, was examined by icv coadministration of alpha-CRH, an antagonist at CRH-1 and CRH-2-receptors. Icv alpha-CRH alone had no intrinsic anxiolytic properties at a dose of 25 microg. The anxiogenic effects of 2 microg CNP icv seen in the plus maze were entirely blocked by alpha-CRH. Directly after exposition ACTH and corticosterone levels did not differ between the groups, but after 30 min ACTH levels were significantly higher in the CNP-treated group compared to alpha-CRH/CNP-treated animals. Corticosterone was found significantly lowered in the alpha-CRH/saline group compared to the CNP treated group but not compared to saline controls. Our data suggest opposing effects of CNP and ANP on anxiety-related behavior and neuroendocrine regulation in rats, which appear to be mediated via different receptor occupation and brain regions, and by a CRH-dependent mechanism.
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PMID:Alpha-helical-corticotropin-releasing hormone reverses anxiogenic effects of C-type natriuretic peptide in rats. 1122 88

Endomorphin (EM)-1 and EM-2 are opioid tetrapeptides recently located in the central nervous system and immune tissues with high selectivity and affinity for the mu-opioid receptor. Intracerebroventricular (i.c.v.) administration of morphine stimulates the hypothalamo-pituitary-adrenal (HPA) axis. The present study investigated the effect of centrally administered EM-1 and EM-2 on HPA axis activation. Rats received a single i.c.v. injection of either EM-1 (0.1, 1.0, 10 microg), EM-2 (10 microg), morphine (10 microg), or vehicle (0.9% saline). Blood samples for plasma corticosterone determinations were taken immediately prior to i.c.v. administration and at various time points up to 4 h post-injection. Trunk blood, brains and pituitaries were collected at 4 h. Intracerebroventricular morphine increased plasma corticosterone levels within 30 min, whereas EM-1 and EM-2 were without effect. In addition, pre-treatment of i.c.v. EM-1 did not block the rise in corticosterone after morphine. Corticotrophin-releasing factor (CRF) mRNA and arginine vasopressin (AVP) mRNA in the paraventricular nucleus (PVN) and POMC mRNA in the anterior pituitary were found to be unaffected by either morphine or endomorphins. Since release of other opioids are elevated in response to acute stress, we exposed rats to a range of stressors to determine whether plasma EM-1 and EM-2 can be stimulated by HPA axis activation. Plasma corticosterone, ACTH and beta-endorphin were elevated following acute restraint stress, but concentrations of plasma EM-1-immunoreactivity (ir) and EM-2-ir did not change significantly. Corticosterone, ACTH and beta-endorphin were further elevated in adjuvant-induced arthritis (AA) rats by a single injection of lipopolysaccharide (LPS), but not by restraint stress. In conclusion, neither EM-1 or EM-2 appear to influence the regulation of the HPA axis. These data suggest that endomorphins may be acting on a different subset of the mu-opioid receptor than morphine. The failure to induce changes in plasma EM-ir in response to the chronic inflammatory stress of AA, the acute immunological stress of LPS, or the psychological stress of restraint, argues against an important role for endomorphins in mediating HPA axis activity.
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PMID:Endomorphins and activation of the hypothalamo-pituitary-adrenal axis. 1125 Jun 60

Chronic stress stimulates corticosterone secretion and recruits brain pathways that regulate energy balance (caloric acquisition and deposition) and facilitate hypothalamic-pituitary-adrenal responsiveness to new stressors. We implanted corticosterone or cholesterol bilaterally either near the central nucleus of the amygdala (CeA) or in the prefrontal cortex to determine whether high concentrations of the steroid act at either site, with or without chronic stress. Rats were adrenalectomized and treated systemically with low doses of corticosterone. Half were maintained at room temperature and the other half were exposed to 5 degrees C cold for 5 days before all rats were restrained. There was limited diffusion of corticosterone from brain implants. Corticosterone in prefrontal cortex, but not CeA, decreased plasma insulin and adrenocorticotropic hormone (ACTH) responses to acute restraint in both control and chronically cold stressed rats. Corticosterone implants near CeA decreased the weight of fat depots only in cold; corticosterone implants in prefrontal cortex were ineffective. We conclude that (i) corticosterone inhibits insulin and ACTH secretion by an action in prefrontal cortex but not CeA; (ii) high concentrations of corticosterone secreted during chronic stress alter metabolism through (autonomic) outputs of the CeA and prefrontal cortex in site- and variable-specific fashion; and (iii) the amygdala is a component of a stress-recruited, state-dependent pathway.
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PMID:Corticosterone exerts site-specific and state-dependent effects in prefrontal cortex and amygdala on regulation of adrenocorticotropic hormone, insulin and fat depots. 1144 77

Scientists have been aware of the existence of a complex relationship between stress and the subsequent activation of the hypothalamic-pituitary-adrenal (HPA) axis and the endocrine and neurobehavioral effects of cocaine for many years now. Our research program has focused on the involvement of HPA axis activation in cocaine reinforcement using the intravenous self-administration model. Behaviorally, there are at least three general phases in the etiology of drug self-administration to consider: acquisition, maintenance and reinstatement. We have investigated the role for the HPA axis during each of these three phases. Corticosterone is necessary during acquisition; self-administration does not occur unless this stress-related hormone is increased above a threshold critical for reward. Sensitivity to low doses of cocaine falling on the ascending limb of the acquisition dose-response curve can be augmented by increasing circulating levels of corticosterone, but similar treatments do not affect responding maintained by higher doses. In a similar vein, ongoing, low-dose cocaine self-administration is decreased by drugs affecting the synthesis and/or secretion of corticosterone. When higher doses falling on the descending limb of the cocaine dose-response curve are self-administered, plasma corticosterone can still reach this hypothetical reward threshold even when synthesis is inhibited, and drug intake is not affected. On the other hand, the self-administration of doses falling on both the ascending and descending limbs of the cocaine dose-response curve can each be attenuated by drugs that block central corticotropin-releasing hormone (CRH) receptors. Finally, corticosterone and CRH are also critical for the stress- and cue-induced reinstatement of extinguished cocaine-seeking behavior, demonstrating an involvement of the HPA axis in the relapse to cocaine use as well. Continued investigations into how stress and the subsequent activation of the HPA axis affect cocaine self-administration will likely result in the identification of more effective and efficient treatment for cocaine addiction.
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PMID:The HPA axis and cocaine reinforcement. 1175 Jul 68

1. The increases in corticotropin-releasing hormone (CRH) mRNA following long-term adrenalectomy are associated with low levels of CRH gene transcription, suggesting that glucocorticoids regulate CRH mRNA at the posttranscriptional level. In this study we determined the time course of transcriptional activation after early adrenalectomy by intronic in situ hybridization, and evaluated the effects of glucocorticoids on CRH mRNA stability. 2. Plasma corticosterone was undetectable 3 h after adrenalectomy, but CRH hnRNA increased only by 12 h, and remained elevated for the next 72 h. CRH mRNA increased 18 h after adrenalectomy and reached a plateau lasting from 2 to 6 days, despite very low CRH hnRNA levels. 3. Assessment of CRH mRNA stability, by incubation of slide-mounted hypothalamic sections in an intracellular-like medium at 37 degrees C, prior to measuring CRH mRNA levels by in situ hybridization, revealed a half-life (t1/2) of 11.5 min in sham-operated rats, and a slower decrease adrenalectomized rats (t1/2--26.3 min). Corticosterone administration for 3 days markedly decreased CRH mRNA t1/2 in both sham-operated and adrenalectomized rats (6.5 and 5.0 min, respectively). 4. The data show that adrenalectomy causes transient increases in CRH mRNA transcription, followed by decreases in the rate of CRH mRNA degradation. This suggests that glucocorticoids regulate CRH mRNA at two sites, by inhibiting transcription and by decreasing mRNA stability.
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PMID:Regulation of corticotropin-releasing hormone (CRH) transcription and CRH mRNA stability by glucocorticoids. 1186 Jan 85

Osmotic stimulation has been shown to modify corticotropin responsiveness. We compared the effects of short- and long-term salt loading on pituitary-adrenal activity in control rats receiving tap water and rats submitted to salt loading for 1 day (S1) or 8 days (S8). Corticosterone (B) and adrenocorticotropic hormone (ACTH) plasma levels were determined at 8 a. m. under basal conditions or after immobilization stress for 15 min or corticotropin-releasing hormone (CRH) stimulation. S1 rats showed a similar ACTH response to immobilization, but an increased CRH response. In contrast, S8 rats showed blunted responses after immobilization or CRH stimulation. To evaluate the circadian variation of this inhibitory effect on the stress in the S8 group, immobilization was also performed at 8 p. m. Plasma ACTH and B levels under resting conditions were higher at 8 p. m. than 8 a. m. (p < 0.05) in control and S8 rats. The ACTH response to immobilization in the S8 group was lower than control at both 8 a. m. and 8 p. m. (p < 0.05); however, this reduction was more evident the morning, resulting in an inversion of the diurnal pattern with a higher ACTH response at 8 p. m. In conclusion, short osmotic stimulation results in an increased pituitary response to CRH, whereas prolonged stimulation decreases the pituitary response to CRH and immobilization, showing an interaction between osmoregulation and hypothalamus-pituitary-adrenocortical activity.
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PMID:The opposite effects of short- and long-term salt loading on pituitary adrenal axis activity in rats. 1198 31

The aim of the present study was to evaluate the relationship between corticosterone, body weight, insulin and androstenedione in order to understand the role of adrenal in contributing hyperandrogenism during delayed ovulation in S. heathi. The circulating corticosterone concentration in female S. heathi showed significant seasonal variation. The peak corticosterone concentration observed during August-September coincides with increased feeding activities in S. heathi. The present study noted a seasonal variation in relationship of corticosterone with insulin and androstenedione in S. heathi. An inverse relationship of corticosterone with insulin and androstenedione was found during August to December, but not during January to May. A seasonal variation in the effect of adrenocorticotropic hormone (ACTH) on adrenal corticosterone production in vitro was observed during reproductive cycle. Corticosterone production in vitro by adrenal declined significantly as compared to the control during quiescence in September. The finding suggests that adrenal attained the peak responsiveness to ACTH during September. ACTH significantly enhanced the androstenedione production by the adrenal in vitro during December, when the circulating androstenedione was also high in S. heathi. This suggests that the adrenal may also contribute to hyperandrogenism during the period of delayed ovulation in S. heathi. Further studies are required to reveal the unique pattern of seasonal relationship between corticosterone, insulin and androstenedione in S. heathi.
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PMID:Relationship between corticosterone and body weight, androstenedione and insulin during the period of delayed ovulation in a vespertilionid bat, Scotophilus heathi. 1237 7

Fenfluramine (FEN) is an amphetamine derivative with anorectic properties similar to amphetamine, but without the stimulatory or abuse potential. Administration of FEN produces an immediate release of serotonin as well as inhibits reuptake; ultimately FEN produces a decrease in serotonin stores in the central nervous system. We have previously shown that the administration of FEN to rats results in increased adrenal cortical hormones under resting conditions, without simultaneous elevations in adrenocorticotropin hormone (ACTH). We hypothesized that the adrenal output would be altered following stress and that the altered adrenal output would affect learning and memory, since the adrenal hormones influence learning and memory capability. In this series of experiments, we administered D,L-FEN (15 mg/kg) four times every 2 h on a single day to rats and investigated the effect on hormonal output following forced swim and the effect on sequential learning in the Cincinnati water maze and spatial learning in the Morris maze beginning 3 days after FEN administration. Animals that received FEN had increased corticosterone and aldosterone titers following forced swim relative to control animals, although no differences in ACTH or testosterone were noted. Animals exposed to FEN had lasting deficits in the Cincinnati water maze but not in the Morris water maze, regardless of testing order. These deficits in the Cincinnati water maze appear to be mediated by the elevation in adrenal output since adrenalectomy abolished the effect of FEN. Corticosterone levels were shown to be elevated during the behavioral testing period in animals exposed to FEN.
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PMID:Administration of D,L-fenfluramine to rats produces learning deficits in the Cincinnati water maze but not the Morris water maze: relationship to adrenal cortical output. 1246 Jun 61


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