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)

Moclobemide was compared with imipramine and placebo in the treatment of major depressive episodes in 75 outpatients. The dosage of moclobemide (25 patients) was 300 mg daily for the first 5 days, after which it could be increased to 600 mg. Imipramine (25 patients) was given in a dosage starting with 33 mg and gradually increased to 100 mg/day in the first 5 days, after which it could be further increased; 25 patients received placebo. Both drugs were equally effective as measured by the Hamilton Rating Scale for Depression, the overall assessment of efficacy and the Zung Self-rating Scale, and clearly superior to placebo; there were no significant differences between the 2 active drugs. Moclobemide was better tolerated than imipramine, and was almost comparable to placebo in this respect.
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PMID:Moclobemide, imipramine and placebo in the treatment of major depression. 224 73

Behavioral and biochemical effects of repeated immobilization stress were determined in male Wistar rats. The influence of acute or repeated administration of antidepressant drugs on these effects of stress were also evaluated. It was found that repeated stress (immobilization 3 h/2 degrees C/4 days or various stressors/8 days) reduced basal locomotor activity of rats and prolonged immobility time in Porsolt's despair test. Antidepressant drugs (desmethylimipramine, imipramine, amitriptyline, clomipramine, mianserine), given acutely, restored basal locomotor activity of stressed rats to control level. Desmethylimipramine, imipramine and amitriptyline reduced immobility time in Porsolt's test similarly in control as in stressed rats. However clomipramine, mianserine and trazodone were effective in this test only in stressed rats. Imipramine given for 4 or 8 days (1 h before the stressor) normalized basal locomotor activity. Repeated (for 8 days) various stressors decelerated utilization of noradrenaline (NA) and dopamine (DA) in the brain. Imipramine given once a day for 8 days (1 h before the stressor) normalized brain utilization of catecholamines (CA). It was proposed that depression of basal motility and reduction of CA utilization in the brain induced by repeated stress may be counter acted by antidepressant drugs.
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PMID:Stress-induced depression of basal motility: effects of antidepressant drugs. 227 76

We have used a resting (5 mM K+) or depolarizing (60 mM K+) choline-based medium, and a nondepolarizing sodium-based or choline-based medium, to characterize the inhibitory potential of tricyclic antidepressants against the voltage-dependent calcium channels or the Na(+)-Ca2+ exchange process, respectively, in synaptosomes from rat brain cortex. Imipramine, desipramine, amitriptyline, and clomipramine inhibited net K(+)-induced 45Ca uptake with similar IC50 values (26-31 microM), and this uptake was also inhibited by diltiazem with an IC50 of 36 microM; these results indicate an inhibition of voltage-dependent calcium channels by tricyclic antidepressants. The net uptake of 45Ca induced by Na(+)-Ca2+ exchange was also inhibited by the four tricyclic antidepressants tested, but not by diltiazem; imipramine (IC50 = 94 microM) was a more potent inhibitor of this process than desipramine (IC50 = 151 microM), and the IC50 values of amitriptyline (107 microM) and clomipramine (97 microM) were similar to that of imipramine. Some degree (approximately 25%) of brain calcium channel blockade could be present at the steady-state concentrations of tricyclic antidepressants expected to occur therapeutic use of these compounds to treat depression or panic disorder.
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PMID:Tricyclic antidepressants inhibit voltage-dependent calcium channels and Na(+)-Ca2+ exchange in rat brain cortex synaptosomes. 228 85

3H-Imipramine binding was measured in freshly prepared platelet membranes from 47 drug-free major depressives and 46 healthy controls. Where possible, platelet binding in depressed subjects was repeated following treatment. A significant negative correlation was found between Bmax and assay protein concentration and Bmax values were corrected for this effect. Adjusted Bmax was significantly lower (by 14%) in female depressed patients than in female control subjects, and the difference was of similar magnitude premenopausally and postmenopausally. No such difference was found in males. Kd did not differ significantly between depressed and control subjects. Multiple regression analysis confirmed significant effects on Bmax of presence of depressive illness, age (positive correlation), and season (higher in summer). Within the depressed sample, Bmax was significantly lower in those subjects with obsessional features. Endogenicity (Research Diagnostic Criteria or Newcastle), dexamethasone suppression test result, drug-free interval, family history of depression, depressive psychosis, suicidal ideation, and past history of suicide attempts were not significantly related to Bmax. Paired comparisons revealed no significant effect on Bmax of 6 weeks' treatment with imipramine, maprotiline, or BRL 14342 or of a course of electroconvulsive therapy.
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PMID:3H-imipramine binding to freshly prepared platelet membranes in depression. 254 56

Imipramine is an established treatment for anxiety in adults. Some evidence also exists that it may be beneficial in children. Because of the frequent co-occurrence of anxiety and affective symptomatology in asthmatic children, a pilot study was undertaken to obtain clinical observations on the effects of imipramine on symptoms of asthma as well as those of separation anxiety and depression in children suffering from intractable asthma. The pilot trial was terminated because of medical complications after 6 patients participated.
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PMID:Use of imipramine in children with intractable asthma and psychiatric disorders: a warning. 264 63

Lofepramine is a tricyclic antidepressant that is structurally similar to imipramine and is extensively metabolised to desipramine. In the absence of other major pharmacological effects it appears that its antidepressant activity stems from the facilitation of noradrenergic neurotransmission by uptake inhibition, and possibly by the additional facilitation of serotoninergic neurotransmission. The overall therapeutic efficacy of lofepramine is comparable to that of imipramine, amitriptyline, clomipramine, maprotiline and mianserin in patients with depression of varying severity, and coexisting anxiety. Dry mouth is the most commonly reported side effect of usual therapeutic doses of lofepramine, but the incidence of this and other anticholinergic side effects is less among patients treated with lofepramine than with imipramine. Lofepramine has not been associated with adverse effects on cardiac function even in cases of attempted suicide by overdose. Thus, providing its apparent favourable side effect profile is confirmed in practice, lofepramine may be a valuable alternative for treatment of the depressed patient where a tricyclic is indicated.
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PMID:Lofepramine. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic efficacy in depressive illness. 264 53

3H-p-Aminoclonidine binding to platelets of children and adolescents with major depressive disorder was compared to that of a healthy control population. Significantly higher alpha 2-adrenoceptor Kd and Bmax values were observed in the patient population. 3H-Dihydroalprenolol binding to lymphocyte membranes of the same patient population showed significantly higher beta-adrenoceptor Bmax values than controls. Control females had significantly higher beta-adrenoceptor Kd values than control males, and the female patients had significantly lower beta-adrenoceptor Kd values than control females. 3H-Imipramine binding to platelets of these patients showed significantly higher imipramine Kd values in patients with a suicide attempt, whereas the imipramine Bmax values were significantly increased in patients with major depressive disorder with or without a suicide attempt. We propose that increased platelet alpha 2-adrenoceptor Kd and Bmax values, together with increased platelet imipramine Kd values, may serve as possible biological markers for children and adolescents with major depressive disorder and a tendency toward suicide. Elevated platelet imipramine and lymphocyte beta-adrenoceptor Bmax values may be biological markers for juvenile depression, and decreased beta-adrenoceptor Kd values may be a biological marker for depression in young females.
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PMID:Biological markers in juvenile depression. 283 65

[3H]-Imipramine and [3H]-paroxetine label with high affinity a recognition site which is associated with the serotonergic transporter in blood platelets. The pharmacological profile of [3H]-imipramine and [3H]-paroxetine binding is highly correlated with the potency of drugs to inhibit the uptake of serotonin. Dissociation kinetic experiments suggest that the substrate recognition site for serotonin may be different from the modulatory site which is labeled with [3H]-imipramine or [3H]-paroxetine. The existence of an endocoid acting on the imipramine receptor to modulate the serotonin transporter has been proposed by several laboratories. In clinical studies most laboratories have reported a decrease in Bmax of [3H]-imipramine binding in platelets from depressed untreated patients when compared with matched healthy volunteers. The Bmax of [3H]-imipramine binding in platelets appears to be a state-dependent biological marker in depression.
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PMID:Studies on the serotonin transporter in platelets. 296 77

[3H]Imipramine binding was studied in the prefrontal cortex and putamen of post-mortem brains from control and Parkinsonian subjects. Saturation and inhibition curves showed both high affinity [3H]imipramine binding related to the serotonin uptake mechanism and low affinity binding which was sodium-independent and unrelated to serotonergic uptake. After subcellular fractionation, high affinity [3H]imipramine binding sites were enriched in synaptosomal fractions. In Parkinson's disease, where brain serotonin concentrations are decreased, there was a significant reduction in the density of the high affinity binding in the prefrontal cortex and putamen while the characteristics of the low affinity binding sites remained unchanged. After subcellular fractionation of the putamen of Parkinsonian patients, the decrease in [3H]imipramine binding was found predominantly in the synaptosomal fractions. These results are consistent with a relation between the high affinity [3H]imipramine binding sites and the neuronal serotonin uptake mechanism. Estimation of [3H]imipramine binding could be used as a specific marker for the study of serotonergic innervation in human post-mortem material. The reduction in the density of tricyclic antidepressant binding sites found in cortical and subcortical areas of Parkinsonian brains may be somehow implicated in the depression often seen in patients.
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PMID:High and low affinity [3H]imipramine binding sites in control and parkinsonian brains. 300 4

3H-Imipramine binding to platelets of patients with primary, unipolar major depressive disorder was investigated and compared to that of a normal, healthy control population. No significant differences could be demonstrated between either the Kd or the Bmax values of the two groups. A negative correlation was observed between imipramine Bmax values and the Hamilton anxiety ratings of the depressed patients. Patients who displayed psychomotor retardation tended to have lower platelet imipramine Bmax values than patients with psychomotor agitation. It is suggested that platelet imipramine Bmax values may be a biological marker for subtypes of depression.
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PMID:Imipramine binding sites on platelets of patients with major depressive disorder. 301 18


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