Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Corticotropin-releasing factor (CRF), the hormone responsible for adrenocorticotropin release during stress, is thought to be hypersecreted in depression. Because recent studies suggest that CRF may serve as a neurotransmitter in the major noradrenergic nucleus, locus coeruleus (LC), it was hypothesized that antidepressants interfere with the putative neurotransmitter role of CRF in the LC by either: 1) decreasing release of CRF; 2) pharmacologically antagonizing CRF; or 3) functionally antagonizing CRF by producing effects on LC cells that oppose these of CRF. In order to test this hypothesis, the effects of acute and chronic administration of two antidepressants, a norepinephrine re-uptake inhibitor (desmethylimipramine, DMI) and a serotonin re-uptake inhibitor (sertraline, SER), on LC spontaneous discharge, LC sensory evoked discharge, LC activation by a stressor and LC activation by CRF, were compared in halothane-anesthetized rats. Acute i.v. administration of DMI decreased both LC spontaneous discharge and discharge evoked by repeated sciatic nerve stimulation. In contrast, acute i.v. SER administration decreased only evoked LC discharge rate. Chronic DMI administration (10.0 mg/kg/day, i.p., 21 days) resulted in tolerance to its effects on spontaneous and sensory-evoked LC discharge. However, chronic DMI administration attenuated LC activation by hemodynamic stress, which is thought to require CRF release. LC activation by intracerebroventricular CRF was not altered in the chronic DMI rats. In contrast to DMI, chronic SER (10 mg/kg/day, i.p., 21 days) did not alter LC activation by either stress of CRF. However, the response of LC cells to repeated sciatic nerve stimulation was somewhat enhanced in chronic SER rats. This is an effect that is opposite that produced by CRF.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antidepressant actions on brain noradrenergic neurons. 233 58

Intracerebroventricular (icv) administration of corticotropin-releasing hormone (CRH) or exposure to a restraint stressor causes acute anorexia in rats. However, the effects on food intake of repeated injections of CRH or repeated exposures to restraint stress have not been previously reported. As the effects of these more chronic CRH and stress treatments may be of greater relevance to emerging hypotheses of the pathogenesis of human eating and affective disorders, we measured the changes in food intake and body weight of rats after repeated central injections of CRH. In two experiments using two different daily dosages of CRH and two different schedules of administration, we found that the anorectic effect of CRH decreased over repeated injections. Weight gain was slowed significantly only in the high-dose experiment. Rats may become tolerant to the anorectic effects of CRH delivered by repeated icv injections. These findings have important implications for hypothesized mechanisms of anorexia nervosa and/or depression.
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PMID:The anorectic effects of CRH and restraint stress decrease with repeated exposures. 234 Mar 20

It has been recently demonstrated that sex steroids can negatively regulate beta-endorphin content as well as proopiomelanocortin (POMC) mRNA levels in the rat basal hypothalamus. In order to verify whether or not all the POMC neurons are equally affected by sex steroids, we arbitrarily divided the arcuate nucleus rostro-caudally into four equal portions and used an in situ hybridization technique to evaluate POMC gene expression in these different regions of the arcuate nucleus in the female rat. It was shown that ovariectomy induced an increase in mRNA levels in the most rostral region of the arcuate nucleus, an effect which was reversed by the concurrent administration of estradiol and dihydrotestosterone. On the other hand, estrogen administration to ovariectomized animals produced a marked depression of mRNA levels in all the regions of the arcuate nucleus with the exception of the most caudal one. These results suggest that sex steroids exert their action in subpopulations of POMC neurons.
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PMID:Regulation of proopiomelanocortin messenger ribonucleic acid content by sex steroids in the arcuate nucleus of the female rat brain. 238 58

There are indications to suggest a relationship between low levels of 5-hydroxy-indoleacetic acid (5HIAA) in the cerebrospinal fluid and suicidal behavior. Many depressed patients show an elevated cortisol secretion. As beta-endorphin is derived from the same precursor as ACTH, it is expected that plasma beta-endorphin levels will also rise in depressed patients. We report here a case of severe depression with diurnal variation who showed low CSF 5HIAA prior to his suicide. In contrast, his catecholamine metabolites were 50% above the mean values of other depressed patients. Hormonal measurements, however, showed low cortisol, prolactin and beta-endorphin levels.
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PMID:Diurnal rhythms of plasma cortisol, beta-endorphin and prolactin, and cerebrospinal fluid amine metabolite levels before suicide. Case report. 243 87

Metabolites of selected neurotransmitters (5-HIAA, HVA and DOPAC) and beta-endorphin were measured in the CSF of 39 chronic pain patients and compared to controls. Twelve of the pain patients also fulfilled criteria for major depression. The concentration of 5-HIAA was increased in female but not male pain patients; there was no significant difference in the CSF concentrations of HVA and DOPAC. The presence of depression did not influence the concentrations of neurotransmitters. No correlation was found between the concentrations of monoamine metabolites and beta-endorphin. However, there was a positive correlation between 5-HIAA and HVA in controls and chronic pain patients without depression but not in depressed patients. It is concluded: chronic pain states are associated with elevation of CSF 5-HIAA in female patients; depression abolishes a positive correlation between 5-HIAA and HVA.
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PMID:CSF monoamine metabolites in chronic pain. 244 27

Differences between physically active and sedentary men were tested by profile comparison. The study identifies the relative importance of circulating beta-endorphin (BE), atherosclerotic disease risk (ADR) index, and selected components of emotionality in discriminating between physically active and sedentary men. The subjects were psychologically normal and medically healthy middle-aged men. Jogging activity was the subject classification criterion. The data were collected on selected physiological (treadmill), biochemical (blood collected from resting subjects), and psychological (Eysenck and MMPI) variables. The physical fitness score (PFS) was used as an index of fitness. Physically active men with a high PFS (n = 21), when compared to the sedentary men with a low PFS (n = 15), exhibited lower basal plasma BE, lower ADR, lower anxiety index (AI), and lower MMPI depression score (D). Canonical correlation analysis showed that PFS and BE in one set were correlated with D and neuroticism (NS) in another set of variables. Discriminant function analysis showed that the AI was the most powerful discriminator between the physically active and sedentary men, followed by BE and NS. Interestingly, BE and NS exhibited the same magnitude of discrimination power. The ADR exhibited less discrimination power, relative to AI, BE, and NS. In conclusion, the physically active men, compared to the sedentary men in this study, exhibited lower basal plasma BE, which appeared to be associated with less atherosclerotic disease risk, less neuroticism, less anxiety, and less depression.
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PMID:Beta-endorphin and components of emotionality discriminate between physically active and sedentary men. 252 21

An alpha-theta brainwave biofeedfack training program was applied as a novel treatment technique for chronic alcoholics. Following a temperature biofeedback pretraining phase, experimental subjects completed 15 30-min sessions of alpha-theta biofeedback training. Compared to a nonalcoholic control group and a traditionally treated alcoholic control group, alcoholics receiving brainwave training (BWT) showed significant increases in percentages of EEG record in alpha and theta rhythms, and increased alpha rhythm amplitudes. Alcoholics receiving BWT showed a gradual increase in alpha and theta brain rhythms across the 15 experimental sessions. These experimentally treated alcoholics showed sharp reductions in self-assessed depression (Beck's Depression Inventory) compared to the control groups. Alcoholics receiving standard medical treatment (abstinence, group psychotherapy, antidepressants) showed a significant elevation in serum beta-endorphin levels at the conclusion of the experiment. This neuropeptide is an index of stress and a stimulant of caloric (e.g., ethanol) intake. Application of brainwave treatment, a relaxation therapy, appears to counteract the increase in circulating beta-endorphin levels seen in the control group of alcoholics. 13-month follow-up data indicate sustained prevention of relapse in alcoholics that completed alpha-theta brainwave training.
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PMID:Alpha-theta brainwave training and beta-endorphin levels in alcoholics. 252 76

In a previous study in unanesthetized goats, we demonstrated that cerebrospinal fluid levels of beta-endorphin were significantly elevated after 2.5 h of inspiratory flow-resistive loading. Naloxone (NLX) (0.1 mg/kg) administration partially and transiently reversed the tidal volume depression seen during loading. In the current study, we tested the hypothesis that endogenous opioid elaboration results in depression of respiratory output to the diaphragm. In six studies of five unanesthetized goats, tidal volume (VT), transdiaphragmatic pressure (Pdi), diaphragmatic electromyogram (EMGdi), and arterial blood gases were monitored. A continuous NLX (0.1 mg/kg) or saline (SAL) infusion was begun 5 min before an inspiratory flow-resistive load of 120 cmH2O.l-1.s was imposed. Our data show that the depression of VT induced by the load was prevented by NLX as early as 15 min and persisted for 2 h. At 2 h, Pdi was still 294 +/- 45% of the base-line value compared with 217 +/- 35% during SAL. There was no difference in EMGdi between the groups at any time. However, the augmentation of Pdi was associated with a greater increase in end-expiratory gastric pressure in the NLX group. We conclude that the reduction in VT and Pdi associated with endogenous opioid elaboration is not mediated by a decrease in neural output to the diaphragm, but it appears to be the result of a decrease in respiratory output to the abdominal muscles.
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PMID:Naloxone alters the early response to an inspiratory flow-resistive load. 253 92

Patients with anorexia nervosa have neuroendocrine and behavioral alterations that starvation and weight loss are thought to cause, or contribute to, since they are reversed by weight restoration. We have found that anorexics have starvation-related disturbances of neuropeptide Y (NPY), corticotropin-releasing hormone (CRH), and beta-endorphin, as determined by their measurements in cerebrospinal fluid. The relationship between these neuropeptides and several symptoms in anorexia, together with findings in experimental animals, raise a possibility that changes in the activity of these neuropeptides contribute to neuroendocrine and behavioral alterations in anorexia. Specifically, a disturbance of central nervous system CRH activity is likely to be responsible for hypercortisolemia, while a disturbance of central nervous system NPY may contribute to amenorrhea. In addition, disturbances of these neuropeptides could contribute to other symptoms such as increased physical activity, hypotension, reduced sexual interest, depression, and pathological feeding behavior.
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PMID:Contribution of CNS neuropeptide (NPY, CRH, and beta-endorphin) alterations to psychophysiological abnormalities in anorexia nervosa. 253 90

The effect of endogenous pituitary and pancreatic beta-endorphins in the physiopathologic factors of acute pancreatitis and the effect of opiate antagonist naloxone in these conditions were studied. Pancreatitis was induced by the injection of 0.5 milligram per kilogram of autologous bile mixed with 10,000 units per kilogram of trypsin into the main duct after ligating the accessory duct. After the induction of acute pancreatitis, plasma beta-endorphin concentrations in systemic and portal blood and cardiovascular function were measured. Ten dogs (control group) were given an intravenous injection of 10 milliliters per kilogram per hour of lactate Ringer's solution one hour before the induction of acute pancreatitis. Six (naloxone group) received an intravenous bolus injection of 2 milligrams per kilogram of naloxone at one hour after the induction of acute pancreatitis and then an intravenous infusion of 2 milligrams per kilogram per hour of naloxone was given under the same conditions as for those in the control group. Beta-endorphin in systemic and portal venous blood in those in the control group increased significantly during the experiments. Beta-endorphin and adrenocorticotropin hormone in systemic venous blood both in the control and naloxone groups increased simultaneously. However, blood pressure, pulse pressure and cardiac output improved quickly after the bolus injection of naloxone and were well maintained during intravenous infusion of naloxone. Also, naloxone improved the survival time from acute pancreatitis and decreased plasma lactate concentrations. Our data show that beta-endorphin, released mainly from the pituitary gland and not from the pancreas, may have an important role in subsequent cardiovascular depression. Also the opiate antagonist naloxone may be effective in the treatment of acute pancreatitis.
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PMID:Plasma beta-endorphin and the effect of naloxone on hemodynamic changes during experimental acute pancreatitis in dogs. 254 May 37


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