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)

Ninety-one female bulimic outpatients received lithium carbonate or placebo on a random basis, after being separated into depressed and nondepressed subgroups, in an 8-week double-blind trial. Sixty-eight patients who completed the study experienced a significant decrease in bulimic episodes after the 8 weeks. Lithium, in a dosage yielding relatively low plasma levels, was not more effective than placebo. However, depression and other psychopathologies decreased with improvement in bulimic behavior.
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PMID:Treatment of bulimia nervosa with lithium carbonate. A controlled study. 190 8

This study was aimed at investigating the effects of treatment with a lithium-imipramine combination on the activity of adenylate cyclase in membranes from the cerebral cortex of the rat. Treatment with (1) lithium for 2 weeks, yielding a level of lithium in serum of 0.54 +/- 0.12 mmol/l, (2) imipramine for 4 weeks (10 mg/kg i.p. twice per day) and (3) a combination of the two drugs reduced isoprenaline-induced stimulation of adenylate cyclase by GTP, with a greater decrement with the combined treatment. None of the treatments exerted any effect on the activity of the enzyme stimulated by GTP alone. Lithium ex vivo inhibited the calcium (Ca2+)- and Gpp(NH)p-stimulated activity of adenylate cyclase, but imipramine ex vivo did not affect the activity of adenylate cyclase, stimulated by these activators. The lithium-imipramine treatment reduced Ca2(+)- and Gpp(NH)p-stimulated activity of adenylate cyclase, but this was not different from that observed in the lithium-treated group. In conclusion, the beta-adrenoceptor-stimulated adenylate cyclase was affected markedly by administration of lithium and imipramine together. In contrast to lithium ex vivo, imipramine ex vivo did not impair the activity of either the guanine nucleotide regulatory protein or the catalytic subunit, since no change in activity was observed in the presence of beta,gamma-imidoguanosine-5' triphosphate (Gpp(NH)p) or Ca2+. Furthermore, lithium ex vivo exerted its post-receptor effects on the adenylate cyclase, independent of imipramine. The decrement in activity of beta-adrenergic adenylate cyclase, induced by administration of the two drugs together may partly be involved in the therapeutic action of the augmentation of antidepressants by lithium in refractory depression.
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PMID:Effects of treatment with a lithium-imipramine combination on components of adenylate cyclase in the cerebral cortex of the rat. 210 75

Lithium augmentation of antidepressant treatment is a commonly used strategy for treatment-resistant cases of depression. Two cases are described in which significant neurotoxicity developed in elderly patients despite therapeutic doses of antidepressant and lithium.
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PMID:Toxicity resulting from lithium augmentation of antidepressant treatment in elderly patients. 238 Jan 60

Lithium enjoys wide clinical use in the treatment of affective disorders, but the mechanism of its action in these conditions is still controversial. Recent studies have shown that lithium can interact with other antidepressant drugs to enhance their efficacy, perhaps by specific effects on serotonin (5-HT) function. A large body of independent evidence suggests that 5-HT function is abnormal in depression. This review documents preclinical evidence of lithium's effects on 5-HT function at the levels of precursor uptake, synthesis, storage, catabolism, release, receptors, and receptor-effector interactions. The weight of this evidence suggests that lithium's primary actions on 5-HT may be presynaptic, with many secondary postsynaptic effects. Studies in humans, using very different methodological approaches, generally suggest that lithium has a net enhancing effect on 5-HT function. These actions of lithium may serve to correct as-yet unspecified abnormalities of 5-HT function involved in the pathogenesis of depression.
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PMID:Lithium and serotonin function: implications for the serotonin hypothesis of depression. 240 94

The effects of short-term (3-4 days) lithium treatment on the prolactin responses to intravenous clomipramine (0.1 mg/kg), metoclopramide (5 micrograms/kg) and haloperidol (2.5-5 micrograms/kg) were assessed in male volunteers. Prolactin responses to clomipramine were significantly enhanced by lithium while those following administration of haloperidol and metoclopramide were not significantly altered. Lithium did not change the cortisol response to clomipramine. The results suggest that lithium may selectively enhance 5-HT mediated prolactin release. These data are consistent with the hypothesis that synergistic effects of lithium and clomipramine on brain 5-HT function may be involved in their therapeutic effect in resistant depression.
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PMID:Lithium increases 5-HT-mediated prolactin release. 250 66

The routine handling of rats and the injection of saline is a stressor. The authors report that chronic twice daily injections of normal saline (1 ml/kg IP) for 14 days produced subsensitivity to the hypothermic effects of nicotine (1 ml/kg IP). The weekly injection of nicotine (1 mg/kg IP) does not produce this effect. The investigators propose that their findings reflect the effect of chronic stress on a nicotinic mechanism. Lithium, desipramine, fluoxetine, and amitriptyline also alter the thermic response to systemically injected nicotine. A nicotinic mechanism(s) may be involved in the neurobiology of chronic stress, actions of antidepressants, and conceivably the pathophysiology of depression.
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PMID:Chronic injections of saline produce subsensitivity to nicotine. 262 80

Lithium, a widely used substance for treatment of manic-depressive illness has been reported to alter the phase relationship of a variety of circadian rhythms which have been implicated in the aetiology of depression and manic-depressive disorder. Although its mechanism of action is not understood, the theraputic action of lithium has been related to its ability to alter circadian rhythms. Chronic lithium administration to rats resulted in lithium levels comparable to the human theraputic range. These lithium levels affected a broad range of biological variables by significantly modifying their circadian pattern of variation, notably during the dark period of an alternating 12h light/12h dark schedule. These included water intake, body weight, retina weight and pineal, serum, retina and hypothalamic melatonin measures. Retinal lithium levels were significantly higher than serum lithium levels and retinal melatonin levels were reduced by lithium. The data are interpreted as suggesting that lithium may exert its theraputic effects by influencing melatonin levels at several locations along the retinal-hypothalamic-pineal pathway, resulting in a modulation of the potential cue value of this physiological stimulus for synchronization of circadian rhythms. Such an effect of lithium could have important chronobiological implications for circadian rhythms which use light and dark as a phase cue.
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PMID:Lithium and circadian patterns of melatonin in the retina, hypothalamus, pineal and serum. 281 53

In this retrospective study the authors determined the efficacy of lithium added to a combined antipsychotic-antidepressant drug regimen in 21 psychotically depressed patients who had been refractory to combined drug treatment. Response to lithium was then compared with response rates of 15 patients to ECT, the established treatment for nonresponsive delusional depression. Lithium was effective in eight of nine patients with bipolar depression but in only three of 12 patients with unipolar depression; ECT was effective in nine of 15 patients with unipolar depression. Lithium augmentation appeared to be a realistic treatment alternative for refractory bipolar patients but was disappointing in unipolar patients.
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PMID:Lithium augmentation in psychotic depression refractory to combined drug treatment. 286 1

Lithium, by inhibiting inositol phosphate metabolism, interferes with the phosphatidylinositol ("phosphoinositide") cycle, which is stimulated by numerous hormones and neurotransmitters. To examine the relevance of this action to neurotransmission, we evaluated effects of lithium treatment on smooth muscle responses to transmitters. In lithium-pretreated tracheal muscle, the relaxation following carbachol or histamine contractions is retarded. Lithium does not affect relaxation following contractions elicited by treatment with KCl and phorbol 12,13-diacetate in combination, which bypasses receptor stimulation of the phosphatidylinositol cycle. Half-maximal effects of lithium occur at 1 mM, corresponding to therapeutic concentrations. Dampening of neurotransmitter responses by lithium treatment may explain the unique ability of lithium to relieve and prevent both mania and depression.
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PMID:Lithium dampens neurotransmitter response in smooth muscle: relevance to action in affective illness. 287 55

Natural killer (NK) cell activity and antibody-dependent cellular cytotoxicity (ADCC) were tested in patients with schizophrenia or depression. It was found that NK activity as well as ADCC were significantly lower in both groups, as compared to healthy control individuals (P less than 0.001). Psychopharmacologic treatment with neuroleptics and antidepressives resulted in a significant increase in NK activity and ADCC (P less than 0.005) in patients with schizophrenia but not in treated patients with depression. In patients with schizophrenia, no correlation could be established between the dose of neuroleptic given and the increase in NK activity. Lithium also did not produce an increase in NK activity and ADCC. The addition of serum, derived from untreated patients with schizophrenia, to cell cultures in concentrations of 10 and 20% had an inhibitory effect upon the ADCC and, to a lesser degree, upon NK activity (20% serum concentration only); sera from treatment schizophrenics produced no inhibition of NK activity, but did affect ADCC. No serum-derived inhibitory effect upon either NK activity or ADCC was found to be present in sera from patients with depression. We conclude that lytic effector mechanisms are impaired in patients with schizophrenia or depression and that this defect is reversed in schizophrenic patients on treatment, but not in depressives on therapy. Patients with schizophrenia also tend to have a reversible serum-mediated inhibition of NK activity which is absent in patients with depression.
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PMID:Lytic effector cell function in schizophrenia and depression. 289 86


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