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)

We evaluated the predictive value of the thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH) in 32 depressed outpatients completing a double-blind placebo-controlled trial of s-adenosyl-l-methionine (SAMe), which failed to show any significant difference between SAMe and placebo. Treatment response was defined as the change in Hamilton Rating Scale for Depression (HRSD-24) score between baseline and the end of the six-week trial. Subjects with TSH response outside the normal range (7-25 uU/ml) had a significantly greater response than patients with a normal response. There was also a significant correlation between absolute deviations from the mean TSH response (16 uU/ml) and changes in HRSD-24 scores.
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PMID:The thyrotropin response to thyrotropin-releasing hormone as a predictor of response to treatment in depressed outpatients. 141 98

Examination of the neurobiology of psychiatric illness in general, and of affective disorders in particular, reveals a variety of associated biochemical abnormalities. These have generally been assumed to be part of the pathological process or secondary to it, and thus deserving of therapeutic efforts aimed at reversal. However, recent clinical and preclinical data suggest that some alterations occurring in the affective disorders may be compensatory and adaptive; that is, part of an endogenous therapeutic mechanism rather than part of the evolving disease process. For example, the symptom of sleep loss in depression seems to fall under this rubric inasmuch as sleep deprivation induces mood improvement in depressed patients. Preclinical data are presented that another primary pathological process--the occurrence of kindled seizures--can evoke endogenous compensatory processes that are either anticonvulsant in their own right, or enable the anticonvulsant effects of a drug such as carbamazepine. It may be that some biochemical abnormalities occurring in affective illness are similarly adaptive. As one example, increased thyrotropin-releasing hormone (TRH) has been reported in the cerebrospinal fluid (CSF) of depressed patients. This elevation of TRH and the resulting neuroendocrine profile may be part of an endogenous counter-regulatory process aimed at mood improvement. Again, preclinical seizure models are supportive in that TRH not only is induced following repeated seizures, but also exerts anticonvulsant effects on these same seizures. In an analogous fashion, TRH elevations in depressed patients may also exert ameliorating effects on depressive symptomatology. This formulation presents directly testable hypotheses that could importantly impact on our understanding of the pathophysiology of affective disorders, and suggests novel therapeutic strategies through the enhancement of endogenous compensatory mechanisms.
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PMID:Ziskind-Somerfeld Research Award 1992. Endogenous biochemical abnormalities in affective illness: therapeutic versus pathogenic. 144 65

Cerebrospinal fluid concentrations of corticotropin-releasing hormone (CRH), thyrotropin-releasing hormone (TRH) and somatostatin (SRIF) were measured in 77 female inpatients with moderate to extreme dementia and in 17 elderly female controls. Both multi-infarct (MID) and Alzheimer-type (SDAT) demented patients had equally elevated CSF CRH and TRH but not SRIF levels as compared with the controls. This elevation was, however, not seen in patients with simple dementia while it was most prominent in those exhibiting marked depressive symptoms. It is concluded that depression rather than dementia itself may be associated with CSF CRH and TRH elevation in elderly patients with cognitive impairment.
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PMID:Cerebrospinal fluid neuropeptides in dementia. 148 50

We investigated the relationship between suicidality, agitation, panic attacks, and the thyrotropin-stimulating hormone (TSH) response to thyrotropin-releasing hormone (TRH), and tested the hypothesis that panic would account for the association between a reduced TSH response and the other conditions. Twenty-seven euthyroid primary unipolar depressed inpatient women received a TRH test and systematic psychiatric assessment. Panic attacks were insufficient to explain the link between the TSH response and suicidal intent, lethality, and agitation; each condition was independently associated with a lower TSH response. In an additive fashion, copresence of conditions further reduced TSH response. The symptom constellation of panic, agitation, and suicidality in depression may correlate with the greatest reduction in TSH response.
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PMID:Panic, suicide, and agitation: independent correlates of the TSH response to TRH in depression. 826 37

We characterized the effects of thyrotropin-releasing hormone (TRH; 500 nM) and guanosine 5'-0-3-thiotriphosphate (GTP gamma S; 50 microM) on two types of Ca2+ currents in pituitary-hormone-secretory GH3 cells and were surprised to find marked increases in transient, low-threshold Ca2+ currents (T currents) induced by extracellularly applied TRH or intracellularly applied GTP gamma S. The effect of TRH was blocked by intracellularly applied guanosine 5'-0-2-thiodiphosphate (GDP beta S; 100 microM). The increase in the T current was found to be accompanied by a decrease in long-lasting, high-threshold Ca2+ current (L-current), in response to both TRH or GTP gamma S. These indicate that the enhancement of Ca2+ influx by TRH (500 nM) is largely conferred by T currents in GH3 cells. A reduced concentration of TRH (5 nM) still markedly increased the T current, but failed to decrease the L current. These data suggest that the augmentation of the T currents as well as depression of the L currents by TRH (500 nM), through the activation of a GTP-binding protein, may constitute an important regulatory mechanism of sustained pituitary hormone secretion in GH3 cells.
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PMID:Augmentation of transient low-threshold Ca2+ current induced by GTP-binding protein signal transduction system in GH3 pituitary cells. 152 Mar 44

Baseline thyroid-secreting-hormone (TSH)-assessed by means of ultrasensitive assays (IRMA)-and free-thyroid-hormone (FT4) levels were determined in 84 depressed females, and the TSH responses to 200 micrograms thyrotropin-releasing hormone (TRH) (IV) measured. It was found that TRH-induced TSH responses were linearly and positively related to basal TSH-IRMA; lower TRH-stimulated TSH secretion in melancholic patients was attributable to lowered basal TSH-IRMA values. A progression was found-within the euthyroid range-of basal TSH-IRMA values towards lower levels along the diagnostic spectrum: the highest basal TSH-IRMA levels were witnessed in minor depressives and the lowest in melancholics, while simple major-depressed females occupied an intermediate position. This shift appears to be indicative of severity of illness. Basal TSH-IRMA data can roughly be used as a clinical tool separating melancholia from minor depression: at a threshold value of less than or equal to 1 microUI/ml, sensitivity was 56% and specificity 92%. It is concluded that basal TSH-IRMA provides a more accurate representation of melancholia than peak TSH responses, which appear to constitute little more than a magnified, but biased signal of basal TSH-IRMA. In future, the assay of basal TSH-IRMA could replace TRH testing.
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PMID:TSH responses to TRH as a function of basal serum TSH: relevance for unipolar depression in females--a multivariate study. 163 32

Previous behavioural and electrophysiological studies have indicated an antinarcotic action of thyrotropin-releasing hormone (TRH) and its analogues in antagonizing the action of CNS depressant drugs, including baclofen and a variety of anesthetics. While beta-adrenergic receptors are implicated in the level of anaesthesia/arousal, whether the analeptic action of TRH involves adrenergic systems for its expression is uncertain. The object of the present experiments, therefore, was to examine interactions between adrenergic systems and the anti-anaesthetic effects of TRH analogue CG3703. It was found that pretreatment with the beta-block (+/-)propranolol did not abolish or reduce the ability of CG3703 to antagonize urethane-induced depression of VBT transmission. These results suggest therefore, that beta-adrenergic systems are unlikely to be involved in the anti-anaesthetic effect of the tripeptide.
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PMID:Interactions between adrenergic systems, anaesthetic and TRH analogue induced analeptic effects on VBT transmission. 166 10

Adrenal and nonadrenal sympathetic preganglionic neurones (SPNs) in the intermediolateral nucleus of spinal segments T8-T10 in the cat were compared according to their responses to iontophoretic application of serotonin, substance P, and thyrotropin-releasing hormone (TRH). Responses of both types of SPN to iontophoretic application of serotonin were characterized by an increase in the rate of discharge that was slow in onset (mean +/- SD = 36 +/- 21 s) and prolonged in afterdischarge (115 +/- 70 s) following termination of application. Depression was never observed and responses were similar whether using serotonin at a pH of 3.3 or 4.5, suggesting that the absence of a depressant effect cannot be accounted for by pH, as has been reported with cortical neurones. Iontophoretic application of methysergide resulted in a decrease in the rate of discharge of both types of SPN and blocked the excitatory responses to serotonin. Adrenal and nonadrenal SPNs were excited by iontophoretic application of substance P. Responses of both types of SPN were similar and were characterized by a gradual increase in the rate of discharge that was slow in onset (42 +/- 27 s) and prolonged in afterdischarge (96 +/- 42 s). Finally, adrenal and nonadrenal SPNs were also weakly excited by iontophoretic application of TRH. These responses were slow in onset (48 +/- 27 s) and prolonged in afterdischarge (78 +/- 35 s). These data indicate that serotonin, substance P, and TRH exert excitatory effects on functionally dissimilar sympathetic preganglionic neurones and support the possibility that they may be chemical mediators of synaptic transmission in the intermediolateral nucleus. In addition, these data may be interpreted to support the notion that serotonin, substance P, and TRH are involved in global activation of the sympathetic nervous system.
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PMID:Adrenal versus nonadrenal sympathetic preganglionic neurones in the lower thoracic intermediolateral nucleus of the cat: effects of serotonin, substance P, and thyrotropin-releasing hormone. 169 19

Production of 18, 12-yr-old Angus cows was summarized as the averaged weaning weight deviations of each cow's calves from their like-aged, like-sexed and similarly managed contemporaries. These cows had spent a large part of their productive lives on pastures dominated by endophyte-infected tall fescue, so differences among them in calf production might have been induced partly by differences in susceptibility to fescue toxicosis. Cows were divided randomly into two groups for a 31-d summer feeding trial. In a crossover design, cows were fed 0 or .9 kg per cow per day of endophyte-infected fescue seed. Various traits were monitored to quantify differences among cows in response to the endophyte-infected fescue seed. Baseline serum prolactin concentration was depressed by fescue seed feeding, but differences among cows in the amount of depression were not related to past calf production. Prolactin release in response to thyrotropin-releasing hormone tended to be depressed by fescue, but the response also was sensitive to factors such as ambient temperature. Serum cholesterol and body weight change did not respond significantly to the fescue challenge. The experiment was not successful in unambiguously differentiating among cows in susceptibility to fescue toxicosis or in relating differential susceptibility to past calf production.
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PMID:Variation among Angus cows in response to endophyte-infected fescue seed in the diet, as related to their past calf production. 190 Aug 30

Lidocaine at greater than or equal to 1 mM and procaine at greater than or equal to 2.5 mM exerted dose-dependent inhibition of the increment in [Ca2+]i induced by 100 nM thyrotropin-releasing hormone (TRH) or 30 mM K+ in GH4C1 cells. The rise in [Ca2+]i induced by K+ was more sensitive to this inhibition than that induced by TRH. Lidocaine was more potent than procaine in inhibiting the [Ca2+]i increment induced by secretagogues. Maximal lidocaine inhibition of the TRH-induced [Ca2+]i increment occurred within 15-20 min and a normal response to secretagogues returned within 20 min after removal of lidocaine from the incubation medium. Our data suggest that in GH4C1 cells local anesthetics depress secretagogue-induced intracellular Ca2+ mobilization, depolarization of the cell membrane, and the opening of voltage-dependent Ca2+ channels. This may explain the depression of secretagogue-stimulated hormone secretion induced by these agents.
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PMID:Lidocaine and procaine inhibit the increase in cytosol Ca2+ induced by thyrotropin-releasing hormone or K+ depolarization in GH4C1 cells. 196 46


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