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)

Most of the controlled studies on the efficacy of medical treatments of obsessive-compulsive disorder (OCD) have involved clomipramine, a tricyclic antidepressant reputed to have anti-obsessional properties. To test the possibility that the drug's antidepressant action mediates the reduction of obsessive-compulsive symptoms, we treated 37 OCD patients with imipramine (mean dose = 233 mg/day) or placebo for 6 weeks and assessed improvement on both obsessive-compulsive and depressive symptoms. Imipramine reduced depression in highly depressed OCD patients, but did not affect obsessive-compulsive symptoms in these or in less depressed patients.
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PMID:Effects of imipramine on depression and obsessive-compulsive symptoms. 361 88

The principal finding in this study was that imipramine binding to platelet membranes was lower in a group of ten alcoholics abstinent a mean of 11 days than in a group of ten age- and sex-matched controls (p less than 0.004). The mean (std dev, std error) for imipramine binding in the alcoholic subjects was 718 (110, 37) femtomol/mg platelet membrane protein and 931 (173, 58) femtomol/mg protein in the control subjects. Imipramine binding did not correlate significantly with age, severity of alcoholism, days of abstinence from alcohol, or severity of depression in the alcoholic subjects. Severity of depression did, however, correlate with severity of alcoholism (r = 0.678, p less than 0.03) in the alcoholic subjects in this study. The results of this preliminary experiment suggest that chronic ethanol exposure might affect either the synthesis of imipramine binding sites in megakaryocytes or the structural environment of imipramine binding sites in the platelet membrane. The significance of lower imipramine binding in alcoholics, all of whom expressed some depressive symptoms, remains to be established.
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PMID:Binding of imipramine to platelet membranes is lower in alcoholics than in controls. 362 11

[3H]Imipramine and [3H]paroxetine label with high affinity a site associated with the serotonin transporter in brain and platelets. The maximum binding capacity (Bmax) of [3H]imipramine in platelets is reduced in untreated depressed patients, and it may represent a useful biological marker in depression. The existence of an endogenous ligand acting on the [3H]imipramine-recognition site to modulate the serotonin transporter has been proposed by several laboratories. 5-Methoxytryptoline inhibits [3H]imipramine binding and [3H]serotonin uptake in the nanomolar range. This compound has been reported to occur in the pineal gland, but probably only in trace amounts. While the physiological relevance of 5-methoxytryptoline or a close analogue remains an open question, the possibility exists that the 'endocoid' for the [3H]imipramine-recognition site plays a role in the pathogenesis of depression.
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PMID:Antidepressant-binding sites in brain and platelets. 381 12

The authors present a review of existing literature along with new data regarding the phenomenology, differential diagnosis, course and treatment of panic disorder and agoraphobia. Panic attacks are viewed as central to the development of these disorders, and individual cognitive frameworks contribute to the manner in which a patient's symptoms evolve. An apparent though unclear relation to depressive states is described. Substance abuse may also be a consequence of recurrent panic attacks. A scheme towards differential diagnosis of panic disorder from other psychiatric and medical disorders is proposed. Personality characteristics of these patients vary considerably, but certain factors, such as dependency, are common. Family relations are often strained and assume importance in treatment. Data on the longitudinal course of illness is presented implying a relationship of panic disorder to both depression and stressful life events in many patients. Treatments that thus far seem most effective are pharmacological and behavioural approaches. Imipramine, MAO inhibitors, and alprazolam currently appear to be the most useful medications employed, although other agents may at times be useful alternatives. Dietary interventions, family therapy, and group and individual psychotherapy are also reviewed and discussed as adjunctive therapies in the treatment of panic disorder.
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PMID:Differential diagnosis and treatment of panic disorder: a medical model perspective. 391 78

Forty-five chronic agoraphobics were randomly assigned to treatment by placebo or imipramine in doses up to 200 mg/day for 28 weeks. All patients also had systematic self-exposure homework with an instruction manual. In addition, half of each drug group had therapist-aided exposure and half had therapist-aided relaxation, each totalling three hours. Patients in both drug groups improved substantially and maintained their gains for one year of follow-up. Imipramine had no significant therapeutic effect despite satisfactory plasma levels and significant drug side effects. Patients' low initial Hamilton depression scores might explain the absence of any drug effect. Antidepressants may be ineffective for agoraphobics who have normal mood. Brief therapist-aided exposure improved phobias and panics to a significant but limited extent, and is a useful adjuvant to self-exposure homework, which can be a powerful therapeutic agency by itself.
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PMID:Imipramine and brief therapists-aided exposure in agoraphobics having self-exposure homework. 613 Jul 52

Case histories were reviewed of 25 patients with RDC diagnoses of schizophrenia or schizoaffective disorder who developed a clinical syndrome of depression subsequent to the resolution of their psychotic episodes. Of these patients, 14 were then treated with imipramine and 11 with amitriptyline in addition to their neuroleptic drugs. As a group, the patients did well--48% had a remission of depressive symptoms and an additional 32% improved. Psychotic exacerbation was noted in only one patient. Imipramine seemed more beneficial than amitriptyline in these patients.
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PMID:Response of postpsychotic depression to adjunctive imipramine or amitriptyline. 613 Oct 64

The authors report on 12 men with ischemic heart disease who developed secondary depression following myocardial infarction or coronary artery bypass-graft surgery and were treated with imipramine hydrochloride for 4 weeks. Imipramine had an antiarrhythmic effect, manifested by reduction in premature ventricular contractions during treatment. This drug did not produce clinically significant disturbances in cardiac conduction, but orthostatic hypotension led to early termination of the drug treatment in 1 subject. Imipramine treatment was associated with significant improvement in both observer-rated and patient-rated depression scales.
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PMID:Cardiovascular and antidepressant effects of imipramine in the treatment of secondary depression in patients with ischemic heart disease. 618 Jun 49

Chronic low back pain is a common problem that has been noted in several studies to exist as a component of masked depression. To determine the usefulness of imipramine in the treatment of chronic low back pain, either by a direct action or indirectly via resolution of a depressive equivalent, 50 consecutive patients were entered into a controlled trail that employed serum imipramine and desipramine levels and Beck depression questionnaires. Forty-one patients completed the study, and 48 were used in the statistical analysis. Imipramine had a statistically significant effect over placebo in most, but not all, of the clinical parameters that were measured. A linear relationship between serum drug levels and reported symptoms was not noted. Only 10 of the 50 patients entered into the study were judged clinically depressed and, of these, 7 were depressed according to standard criteria. There was no statistically significant difference noted in either the initial or the change in Beck depression scores between those on imipramine and those on placebo. However, among those on the active drug, the patients with a greater symptomatic response had a simultaneous change in the total Beck depression scores (toward less depression) that approached statistical significance when compared with those with a less symptomatic response. Although the results are not conclusive, imipramine may possibly be useful in the treatment of chronic low back pain, especially so when it exists as a component of masked depression.
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PMID:Controlled trial of imipramine for chronic low back pain. 621 Jul 51

(3H)Imipramine binding sites in the brain are localized mainly on serotonergic nerve terminals. In the hippocampus of rats with a lesion of serotonergic nerve terminals produced by neonatal administration of 5,7-DHT, the depletion of serotonin was paralleled by a decrease in (3H)imipramine recognition sites. (3H)Imipramine recognition sites in brain tissue or platelets are associated with serotonin uptake sites. A significant correlation exists between the potency of a series of antidepressants and other compounds to displace high affinity (3H)imipramine binding and to inhibit the neuronal uptake of serotonin but not of norepinephrine. There is a significant correlation between the ability of drugs to displace (3H)desipramine binding and to inhibit norepinephrine but not serotonin reuptake. (3H)Desipramine recognition sites are located, at least in part, at noradrenergic nerve terminals since destruction of these terminals by 6-OH-DA results in parallel decrease in (3H)desipramine, but not in (3H)imipramine binding. The high affinity recognition sites of (3H)imipramine and (3H)desipramine in the brain could be physiologically and pharmacologically relevant regulatory sites associated with neuronal uptake of serotonin and norepinephrine, respectively. Treatments which clinically lead to improvement of depression (eg. antidepressants, ECT, REM sleep deprivation) were shown to "down-regulate" (3H)imipramine binding sites in brain of experimental animals. The density of (3H)imipramine binding sites was shown to be lower in platelets from depressive patients and in brains of suicide victims. It appears that decreased binding of (3H)imipramine to platelets of depressed patients is a promising biological marker of depression, although there is no conclusive evidence to indicate whether it is a state- or trait-dependent phenomenon.
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PMID:Antidepressant binding: implications for the mode of action and the biology of depression. 632 Feb 97

It has been shown recently that chronic administration of tricyclic antidepressant drugs results in enhanced responsiveness of neurones to iontophoretically applied 5-hydroxytryptamine (5-HT) in rat forebrain regions. The present investigation tested whether this efect is accompanied by an enhancement of behavioral effects of the amine. Behavioral signs of sleep in young chicks following systemic administration of 5-HT were used as an index of the acion of the amine at central receptor sites. Imipramine, desipramine, amitryptiline, pizotifen, and mianserin given 30 min before 5-HT all reduced the duration of 5-HT-induced behavioral depression. However, 6-8 day pretreatment with the same drugs resulted in an increased duration of the 5-HT-induced depression. The results suggest that the antidepressant drugs can block 5-HT receptors in the central nervous system (CNS) and that chronic blockade resulting from repeated administration of the drugs results in an increase in number or sensitivity of 5-HT receptors.
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PMID:Enhancement of 5-hydroxytryptamine-induced behavioral effects following chronic administration of antidepressant drugs. 677 72


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