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)

In an 8-week controlled double-blind clinical trial with a total of 216 patients Brofaromine was found to be superior to Imipramine with regard to efficacy (Hamilton Depression Scale, von Zerssen self-rating scale, global evaluation) and tolerability (adverse experiences, global evaluation). Mean daily dosages were 93.1 mg/day in the Brofaromine group and 92 mg/day in the Imipramine Group. No tyramine reduced diet had to be observed. Long-term efficacy and tolerability also proved to be good in an open follow-up in the Brofaromine group.
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PMID:Brofaromine in major depressed patients: a controlled clinical trial versus imipramine and open follow-up of up to one year. 146 Jan 66

Paroxetine is a novel antidepressant that selectively inhibits neuronal reuptake of serotonin. Results are reported from a 6-week, double-blind trial of paroxetine, imipramine, and placebo in 120 outpatients with DSM-III major depression. Paroxetine was significantly superior to placebo on almost all measures. This included the main outcome variable, the Hamilton Rating Scale for Depression (HAM-D), and its factor scores, anxiety-somatization, cognitive disturbance, psychomotor retardation, and sleep disturbance. There were no significant differences between paroxetine and imipramine on the same scales. Imipramine-treated patients were significantly more likely than those taking placebo to report one or more adverse effects, which were predominantly anticholinergic in nature. There was no significant difference in the number of paroxetine and placebo patients who reported one or more adverse effects. The results of this and similar studies indicate that paroxetine is an effective treatment in major depression and has a favorable side effect profile.
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PMID:A 6-week, double-blind trial of paroxetine, imipramine, and placebo in depressed outpatients. 153 23

Paroxetine is a selective serotonin reuptake inhibitor which is being developed as an antidepressant. Previous studies suggest it is effective in the treatment of depression and has a low incidence of side effects. The authors report on a 6-week, randomized, prospective trial of paroxetine, imipramine, and placebo in 120 outpatients with major depression. The results showed that paroxetine was significantly superior to placebo in relieving depression. There were no significant differences in antidepressant efficacy between paroxetine and imipramine. However, paroxetine was also significantly superior to placebo on several measures of anxiety. Imipramine either was not superior on these measures or took longer to show a significant difference. Paroxetine lacked the typical anticholinergic side effects that accompanied imipramine therapy. The results show that paroxetine is an effective antidepressant that may have value especially when depression is accompanied by significant anxiety.
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PMID:Paroxetine in major depression: a double-blind trial with imipramine and placebo. 153 26

Imipramine is the prototypic tricyclic antidepressant utilized in the treatment of major depression and exerts its therapeutic efficacy only after prolonged administration. We report a study of the effects of short-term (2 wk) and long-term (8 wk) administration of imipramine on the expression of central nervous system genes among those thought to be dysregulated in imipramine-responsive major depression. As assessed by in situ hybridization, 8 wk of daily imipramine treatment (5 mg/kg, i.p.) in rats decreased corticotropin-releasing hormone (CRH) mRNA levels by 37% in the paraventricular nucleus (PVN) of the hypothalamus and decreased tyrosine hydroxylase (TH) mRNA levels by 40% in the locus coeruleus (LC). These changes were associated with a 70% increase in mRNA levels of the hippocampal mineralocorticoid receptor (MR, type I) that is thought to play an important role in mediating the negative feedback effects of low levels of steroids on the hypothalamic-pituitary-adrenal (HPA) axis. Imipramine also decreased proopiomelanocortin (POMC) mRNA levels by 38% and glucocorticoid receptor (GR, type II) mRNA levels by 51% in the anterior pituitary. With the exception of a 20% decrease in TH mRNA in the LC after 2 wk of imipramine administration, none of these changes in gene expression were evident as a consequence of short-term administration of the drug. In the light of data that major depression is associated with an activation of brain CRH and LC-NE systems, the time-dependent effect of long-term imipramine administration on decreasing the gene expression of CRH in the hypothalamus and TH in the LC may be relevant to the therapeutic efficacy of this agent in depression.
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PMID:Long-term antidepressant administration alters corticotropin-releasing hormone, tyrosine hydroxylase, and mineralocorticoid receptor gene expression in rat brain. Therapeutic implications. 167 67

Platelet tritiated imipramine binding values in healthy controls vary considerably from study to study. A possible contributor to such variation might be a circadian rhythm affecting binding, although previous studies of this have been contradictory. Platelet imipramine binding was examined in 12 healthy, medication-free subjects studied at 8 a. m., 11 a. m., 4 p. m., and 10 p. m. during one day. Imipramine binding was determined on platelet membranes, using 0.8-8 nM 3H-imipramine, and nonspecific binding was defined by 50 microM desipramine. All samples from a given individual were assayed simultaneously. The intra-assay coefficient of variation was 6.3 percent. There was no evidence of significant differences in binding capacity or affinity (Bmax or Kd) at different times of day. Circadian variation was explored using COSINOR analysis (DeMet et al., 1989). There was no evidence of circadian variation in binding using this model, even when only the variable portion of binding was considered for each individual. Intraindividual variation in binding was substantial, with a mean coefficient of variation of 29 percent for Bmax and 38 percent for Kd. The possible basis of this variation is unclear, but may reflect the presence of "occult" binding sites in the membrane, or the effect of endogenous modulators of binding. The interrelationship of Bmax and Kd may also be a factor. It was considered that low-affinity binding did not account for a significant part of the variation in Kd in this assay. The utility of imipramine binding as a biological marker of depression may be limited by such levels of intraindividual variation in binding parameters.
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PMID:Circadian variation in platelet imipramine binding during the day in healthy subjects. 189 84

A long-term follow-up assessment was conducted in 25 chronically depressed patients who had participated in a 6-week trial of imipramine to determine if imipramine responders would sustain a more favorable long-term outcome than nonresponders or noncompleters. Imipramine responders tended to remain on imipramine treatment throughout the follow-up interval and had a significantly better outcome. Eighty-nine percent of the imipramine responders met the criteria for recovery at follow-up compared with 31% in the comparison groups. Imipramine responders also fared significantly better at follow-up on measures of depression, global severity of illness, and social/vocational functioning. The results supported a more favorable long-term outcome in chronic depression patients who had responded to imipramine and suggest that maintenance therapy may be indicated and effective for this disorder.
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PMID:Long-term follow-up of chronic depression treated with imipramine. 199 36

The effect of short- and long-term treatment with imipramine and lithium on shock stress-induced escape failures in a shuttlebox (the "learned helplessness" model of depression) was investigated in rats. Acetylcholinesterase (AChE) activity was measured in the frontal cortex, hippocampus and striatum after the shuttlebox test. Imipramine was found to normalize escape behavior, whereas lithium further aggravated escape behavior. No correlation was found between escape behavior and AChE activity in the three brain areas investigated. However, a significant decrease in AChE activity in striatum was found in rats exposed either to shock stress and no drug treatment or to drug treatment and no shock stress. In rats exposed to the combination of shock stress and drug (imipramine or lithium), a slight or no decrease of AChE activity occurred. Exposure to shock stress alone produced no changes in AChE activity in the hippocampus and frontal cortex. In conclusion, lithium did not have an antidepressant effect on "learned helplessness" and AChE activity was not correlated to escape behavior. However, both imipramine and lithium normalized the decreased level of AChE activity in striatum in rats exposed to shock stress.
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PMID:The effect of imipramine and lithium on "learned helplessness" and acetylcholinesterase in rat brain. 201 59

Few clinical reports describe tolerance induced by antidepressants and this question is considered an unsolved problem for clinical use of this group of drugs. The present report deals with the effects of imipramine and mianserine on two animal models of depression, after acute or prolonged previous treatment with these antidepressants. Imipramine and mianserine potentiated amphetamine-induced anorexia both after acute administration or after prolonged previous treatment with each drug. Mianserine effects were not detected in the behavioral despair test and imipramine reduced rats immobility equally after acute and prolonged previous treatment. It was concluded that imipramine and mianserine do not induce detectable tolerance when previously administered to animals submitted to amphetamine anorexia or behavioral despair.
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PMID:Lack of tolerance to imipramine or mianserine in two animal models of depression. 209 93

Imipramine binding to platelet membranes from depressed patients was analyzed. The patients were divided into two groups: one with depression alone, another with depression and psychogenic pain. The depressed patients with psychogenic pain had lower imipramine binding than the depressed patients without pain.
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PMID:Imipramine binding in depressed patients with psychogenic pain. 216 48

Imizine (10 mg/kg, 14 days) was shown to change the temporal dynamics of forced swimming in rats and to decrease the biorhythmical index of depression. The antidepressant also produced reorganization of the circadian rest-activity rhythm with the acrophase shift for the late night hours. A pineal hormone melatonin (1 and 10 mg/kg, 7 days) administered in combination with imizine attenuated the main rhythmic indices of its action and precipitated the occurrence of tolerance.
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PMID:[Attenuation of the effect of imizin on the dynamics of forced swimming and the circadian rhythm of mobility in rats chronically administered melatonin]. 222 51


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