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)

Thyrotropin-releasing hormone (TRH) stimulation tests were performed on 81 alcoholic men after at least 3 weeks of abstinence. Subjects were given 500 micrograms of TRH intravenously, and thyroid-stimulating hormone (TSH) and prolactin (PRL) were measured at baseline, and then 15 and 30 min later. Comparisons were made among alcoholics with (n = 27) and without (n = 54) a lifetime history of depression as determined by the Diagnostic Interview Schedule. Nine nondepressed, nonalcoholic subjects served as controls. Alcoholics with or without a depression history did not differ from each other or from control in TSH or PRL response area under the curve. Blunted TSH responses were present in 10 (12%) of the alcoholics and none of the controls when blunting was defined as a delta max TSH less than 5 microU/ml. When blunting was defined as a delta max TSH less than 7 microU/ml, 18 (22%) of the alcoholics and 1 (1%) of the controls were blunted. Conversely, 2 (2.5%) of the alcoholics had a delta max TSH greater than 32 microU/ml. All subjects were clinically euthyroid. Contrary to expectation, depressed subjects were slightly less likely to show blunted responses than nondepressed subjects. No relationship was found between neuroendocrine measurements and several measurements of alcoholism or depression. Some alcoholic subjects show a blunted TSH response to TRH injection, which may be a function primarily of the alcoholism itself. The precise mechanism remains unknown.
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PMID:Thyrotropin and prolactin response to thyrotropin-releasing hormone in depressed and nondepressed alcoholic men. 210 5

We used a pharmacologic probe that measures the neuroendocrine response to acute, intravenous "challenge" with the serotonin re-uptake inhibitor, clomipramine, in our studies of the biochemical bases of depressive illness. In two studies conducted at different sites, depressed patients consistently demonstrated blunted prolactin responses to clomipramine, compared with healthy control subjects. In order to clarify the mechanisms that might account for this abnormal neuroendocrine response to clomipramine in depression, we administered a thyrotropin-releasing hormone (TRH) stimulation test to 7 depressed patients who had also received a clomipramine challenge test. Although these patients demonstrated blunted prolactin responses to clomipramine, their prolactin responses to TRH were robust. These observations suggest that the blunted prolactin response to clomipramine in depression is not attributable to diminished hormonal secretory capacity in anterior pituitary lactotrophs and may be a reflection of dysregulation in central serotonergic systems.
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PMID:Abnormal neuroendocrine responsivity to clomipramine in depression. 212 36

Biological tests may help clarify the relationship of schizoaffective disorder to major depressive disorder (MDD) and schizophrenia (SCZ). Thyrotropin-releasing hormone (TRH), 500 micrograms, was administered intravenously to eight schizoaffective depressed (SD), ten SCZ, 23 MDD patients and 43 healthy controls (HC), all males, ages 20-66 years and drug-free. Research Diagnostic Criteria (RDC) were utilized for establishing diagnoses, Hamilton Rating Scale for Depression (HRSD) total scores were used for assessing depressive symptoms. There were no differences in dmax PRL (post-TRH prolactin peak minus baseline, mean +/- SD) amongst SD, SCZ and HC groups (27.3 +/- 5.2, 28.8 +/- 5.4 and 31.5 +/- 5.6 ng/ml respectively). Mean dmax PRL in MDD was significantly lower than each of the other three groups (17.1 +/- 2.2 ng/ml, P less than 0.05 for all). The essentially normal PRL response to TRH in SD, significantly different from MDD but similar to SCZ parallels our previous observations on the pattern of thyrotropin (TSH) response to TRH in the same diagnostic groups. These biological findings may be taken to indicate that schizoaffective disorder, depressed subtype, is closer to schizophrenia than to major depressive disorder. However, they cannot be considered definitive evidence to that effect since schizoaffective disorders are known to be quite heterogeneous, and since the utilized biological tests lack specificity.
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PMID:Prolactin response to thyrotropin-releasing hormone in schizoaffective depressed compared to depressed and schizophrenic men and healthy controls. 212 54

The neuropeptides thyrotropin releasing hormone (TRH) and prolactin (PRL), which affect various behaviors in animals, showed "antidepressant" properties in an experimental model of depression. Subcutaneous administration of TRH reduced the total immobility time of rats tested in the despair (constrained swim) test and potentiated the anti-immobility effect of intraperitoneally administered desimipramine (DMI). This effect was not mimicked by the peripheral injection of TSH, T3 or T4. Hyperprolactinemia induced by pituitary homografts under the kidney capsule and the intracerebroventricular injection of PRL also potentiated the DMI-induced reduction of total immobility time of rats in the despair test and exerted "antidepressant" effects in aged rats.
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PMID:Effects of TRH and prolactin in the behavioral despair (swim) model of depression in rats. 212 10

In order to study putative differences in central neurotransmitter function in depressive subtypes, serum cortisol and prolactin responses to the putative serotonin agonist fenfluramine were examined in 30 subjects with major depression. Patients with endogenous depression (melancholia) as defined by each of ICD-9, DSM-III, RDC and Newcastle scale demonstrated a reduced prolactin response to 60 mg oral fenfluramine when compared with non-endogenous subjects. This was independent of either prolactin or cortisol baseline levels, and indicates that there are differences in brain neurotransmitter function in the endogenous and non-endogenous subtypes of depression. Basal prolactin levels were reduced in bipolar compared with unipolar subjects, and delusional compared with non-delusional patients, although there were no differences in the prolactin responses to fenfluramine between these subgroups. Basal cortisol levels and cortisol response to fenfluramine did not distinguish between any of the subtypes.
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PMID:Hormonal responses to fenfluramine in depressive subtypes. 213 Nov 37

To investigate central neurotransmitter function in depression, baseline levels of serum cortisol and prolactin and the responses of these hormones to the putative serotonin agonist fenfluramine (60 mg, oral) were examined in 27 depressed patients and 14 normal subjects. Baseline cortisol was significantly elevated (P less than 0.01) in depressed subjects, whilst baseline prolactin was significantly reduced (P = 0.01) after covarying for cortisol. Although there were no significant abnormalities in either the prolactin or the cortisol response to fenfluramine in the total depressed group, the peak increase in prolactin levels (delta PRL) was significantly reduced (P less than 0.05) in subjects with endogenous depression. Analysis of covariance demonstrated, however, that the reduced delta PRL was partially dependent upon the abnormal baseline prolactin and cortisol levels. These results indicate the necessity of accounting for these baseline effects when investigating hormonal responses to the putative serotonergic challenges. The abnormal baseline findings are consistent with increased central noradrenergic activity in depression.
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PMID:Hormonal responses to fenfluramine in depressed and control subjects. 214 Aug 46

Fifty-five male patients who had suffered a mild head injury 11-13 months previously were investigated for evidence of depression. Eleven were diagnosed as DSM-III major depressives, nine with melancholia. Prolactin response to buspirone was examined in these patients, in eight male head-injured patients without depression and 10 age-matched male healthy controls. The prolactin response was significantly blunted in post head injury depressed patients compared to head injury non-depressed and healthy control groups. We suggest that these differences may be due to altered serotonin functioning post head injury.
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PMID:Buspirone/prolactin response in post head injury depression. 214 99

The chemistry, pharmacology, pharmacokinetics, adverse effects, and dosage of clomipramine hydrochloride are described, and clinical studies of the use of clomipramine in treating obsessive-compulsive disorder (OCD), other psychiatric conditions, and chronic pain are reviewed. Clomipramine hydrochloride, a tricyclic antidepressant, is a potent inhibitor of serotonin reuptake and may affect dopaminergic neurotransmission, suppress rapid eye movement sleep, produce changes in electrocardiograms, and elevate plasma prolactin. The drug is well absorbed from the gastrointestinal tract and undergoes extensive first-pass metabolism. Peak plasma concentrations occur three to four hours after a 150-mg oral dose. The mean elimination half-life is 39 hours. Some 66% of a dose is excreted in the urine, the remainder being eliminated in the feces. In clinical trials, clomipramine was significantly more effective than placebo, clorgiline, amitriptyline, imipramine, and doxepin in ameliorating the symptoms of OCD. Initial effects are seen at four weeks; improvement may continue for up to 18 weeks. Clomipramine may also be effective in treating panic attacks, phobias, depression, and chronic pain. The most common adverse effects of clomipramine are anticholinergic; others include nausea, seizures, and sexual difficulties. Interactions between clomipramine and barbiturates, haloperidol, monoamine oxidase inhibitors, and cigarette smoking have been documented. The usual initial adult dosage is 25-50 mg/day, titrated gradually to 250 mg/day if necessary. Clomipramine hydrochloride is a welcome new agent for the treatment of obsessive-compulsive disorder. Although its adverse-effect profile is like that of other tricyclic antidepressants, sexual dysfunction and seizures may be more frequent with this agent and limit its use.
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PMID:Clomipramine: an antiobsessional tricyclic antidepressant. 218 Jun 23

In view of evidence that brain serotonin (5-HT) function is abnormal in depression, the ability to alter 5-HT function has been studied as a mechanism of antidepressant drug action. In preclinical studies, antidepressants had significant effects on 5-HT receptor sensitivity. In the clinical setting, the pharmacologic challenge paradigm has generated interest as a means of studying 5-HT function. Most frequently used in these studies has been intravenous L-tryptophan (L-TRP), which increases serum prolactin (PRL). The authors review the neuroendocrine effects of intravenous L-TRP in depression and other conditions, as well as the effects of thymoleptic drugs on the PRL response to L-TRP. Findings are discussed in light of recent evidence that experimentally reduced plasma TRP can reverse the therapeutic effects of some antidepressants.
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PMID:Clinical data on the role of serotonin in the mechanism(s) of action of antidepressant drugs. 218 16

To examine further the serotoninergic system in obsessive-compulsive disorder (OCD), the plasma concentrations of cortisol and prolactin and the behavioral responses after oral administration of MK-212 (6-chloro-2-[1-piperazinyl]-pyrazine), a serotonin agonist, and placebo were studied in 17 patients with OCD and nine normal controls. The two groups did not differ significantly in basal plasma prolactin or cortisol levels. Nevertheless, both the prolactin and cortisol response to oral administration of MK-212 (20 mg) were significantly blunted in the patients with OCD compared with those of the normal controls. MK-212 did not affect the intensity of OCD symptoms. However, MK-212, as compared with placebo, produced slight but statistically significant increases in self-ratings of nausea, dizziness, anxiety, feeling strange, and mixed feelings of calmness and restlessness, as well as depression and feeling high. These behavioral ratings were not significantly different in patients and normal controls. These findings are consistent with previous reports of diminished serotoninergic responsivity in OCD and raise the possibility of subsensitivity of at least some serotonin receptors in this disorder.
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PMID:Prolactin and cortisol responses to MK-212, a serotonin agonist, in obsessive-compulsive disorder. 220 27


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