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)

Imipramine has been shown to have a potent inhibitory effect on sperm motility in vitro. Because of the frequent chronic use of antidepressants in treatment of depression, we investigated the in vivo effects of desmethylimipramine and lithium carbonate on sperm function in patients suffering from clinical depression. We also studied the in vitro effects of a series of neurotrophic agents on sperm motility. There were no significant differences in sperm count, viability, or motility between a group of patients diagnosed as having clinical depression and a group of semen donors with normal sperm characteristics. Three weeks of continuous therapy with desmethylimipramine or lithium carbonate resulted in a significant decrease in sperm viability but no significant change in sperm count or motility. The in vitro drug studies demonstrated that imipramine hydrochloride, desmethylimipramine, chlorpromazine, trifluoperazine, and nortriptyline hydrochloride were all potent inhibitors of sperm motility, whereas lithium carbonate had no effect on motility.
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PMID:Effects of psychotropic drugs on human sperm motility. 679 7

Effects of the drugs affecting monoaminergic neurotransmission were examined on the spinal polysynaptic reflex (PSR) in anesthetized spinal rats. Chlorpromazine HCI (0.5-2.0 mg/kg, i.v.) and baclofen (0.63-2.5 mg/kg) depressed and imipramine HCI (1.25-5.0 mg/kg) increased the amplitude of PSR in acute spinal animals, recorded as evoked electromyogram in the gastrocnemius muscle by electrical stimulation of the common peroneal nerve. However, chlorpromazine and imipramine showed effects neither on PSR in chronic spinal rats, nor in acute spinal rats with the intracisternal administration of 6-hydroxydopamine, which caused depletion of the spinal noradrenaline, dopamine and serotonin, and selective depletion of the spinal noradrenaline, respectively. Baclofen depressed the amplitude of PSR in both preparations with almost the same potency as that in acute spinal ones. Imipramine HCI (2.5 mg/kg, i.v.), chlorpromazine HCI (1.0 mg/kg) and baclofen (1.25 mg/kg) depressed the mono- and polysynaptic heights of the ventral root potentials in acute spinal rats. However, their depression of polysynaptic height was not so strong. These observations strongly suggest that, at the receptor sites on spinal interneurons where the descending monoaminergic neurons terminate, spinal monoamines, especially noradrenaline, are involved in PSR modification by chlorpromazine and imipramine, but not in PSR depression by baclofen.
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PMID:Effects of chlorpromazine, imipramine and baclofen on the spinal polysynaptic reflex in acute, chronic and 6-hydroxydopamine-treated spinal rats. 681 74

Pulmonary amine extraction (E) was measured by triple-indicator dilution techniques from bolus injections of trace amounts of 5-hydroxy[14C]tryptamine ([14C]HT)m [3H]norepinephrine ([3H]NE), indocyanine green dye before and after glass-bead embolization in 23 anesthetized dogs. Control E(5-[14C]-HT) was 89.7 +/- 1.7%; 10 min after embolization (which approximately doubled pulmonary artery pressure and pulmonary vascular resistance), E(5-[14C]HT) was significantly reduced to 65.9 +/- 3.0% (kappa +/- SE; n = 10) (P less than 0.01). Control E([3H]NE) (40.1 +/- 4.5%) was unaffected by embolization. Imipramine (8 mg/kg) depressed control E(5-[14C]HT) to 38.7 +/- 1.5% and control E([3H]NE)d to 35.0 +/- 3.9% (P less than 0.05; n = 4). In these animals, pulmonary hemodynamic changes secondary to embolization were comparable to those in non-drug-treated dogs, but E(5-[14C]HT) and E([3H]NE) were not further depressed. Progressive pulmonary lobar artery ligation (n = 5) did not affect amine extraction until perfusion was limited to one lobe. The selectivity of the effect of embolization on E(5-[14C]HT), the lack of an effect on imipramine-insensitive E(5-[14C]HT) extraction, and the much smaller changes after progressive lobar ligation indicate that, although derecruitment of vascular surface area secondary to mechanical obstruction may contribute to postembolization depression of E(5-[14C]HT), additional mechanisms such as local saturation of 5-HT uptake or selective damage to endothelial cell transport of 5-HT may underlie these observations.
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PMID:Selective effect of microembolization on pulmonary removal of biogenic amines. 706 Dec 95

The disposition of orally administered imipramine (IMI) was studied in 11 depressed alcoholic and 12 depressed nonalcoholic male inpatients. Subjects received 50 mg three times daily for at least 10 days to ensure steady state. Following a temporary discontinuation of therapy, several blood samples were drawn over a 40-hour period. Imipramine, desipramine, and their 2-hydroxylated metabolites were measured in plasma using a high performance liquid chromatography assay. Eight hours following the last dose, alcoholics has significantly lower IMI (50 +/- 41 versus 106 +/- 46 ng/ml; p less than 0.005) and 2-hydroxyimipramine (12.8 +/- 7.5 versus 22.6 +/- 9.8 ng/ml; p less than 0.01) levels than controls. The mean terminal half-lives in the two groups were nearly identical (16.3 +/- 6.7 hours in alcoholics versus 17.1 +/- 5.4 hours in controls). Beck Depression Inventory scores were significantly reduced during IMI therapy (p less than 0.001) in the non-alcoholic controls, whereas no change was observed in the alcoholic group. These results are consistent with either a decrease in oral bioavailability of IMI in alcoholics or, assuming complete absorption, an increase in intrinsic clearance of 2.5 fold (2444 +/- 1151 versus 986 +/- 438 ml/min; p less than 0.005) over the clearance found in control subjects. The latter seems a more likely result of chronic ethanol intake. The fact that lower levels of IMI in the alcoholic group were accompanied by a lack of efficacy in relieving depressive symptomatology suggests that whether through an effect on bioavailability or intrinsic clearance, ethanol consumption is an important consideration when recommending tricyclic therapy.
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PMID:Imipramine disposition in alcoholics. 706 40

18 hospitalized male depressives were treated with imipramine hydrochloride for 28 days. Prior to initiating treatment, each patient completed the Minnesota Multiphasic Personality Inventory (MMPI). At the end of the treatment period, the patients were divided into groups of responders and nonresponders based on the change in their Hamilton Depression Rating Scale scores. The Imipramine Response Scale - Male (IRS-M) was scored for each patient and the ability of the scale to predict response or nonresponse in our sample of patients was examined. There was no evidence that the IRS-M was better than chance in its ability to predict response.
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PMID:MMPI prediction of imipramine response: a replication study. 745 54

The involvement of opioid system on the learned helplessness model of depression was investigated. Animals preexposed to inescapable shocks were treated with either Met-enkephalin, Leu-enkephalin, morphine, imipramine, naloxone, RB 38A (a mixed inhibitor of enkephalin degrading enzymes), or RB 38B (a selective inhibitor of neutral endopeptidase EC 3.4.24.11). Stimulation of opioid system by either opioid agonists or enkephalin catabolism inhibitors reversed the escape deficit induced by shock pretreatment. In contrast, administration of naloxone potentiated the effect of inescapable shocks. Imipramine reduced the number of escape failures in this test, and this effect was antagonized by naloxone. These results point to the involvement of the endogenous opioid system in this model of depression.
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PMID:Implication of endogenous opioid system in the learned helplessness model of depression. 750 57

The interactions between Ca(2+)-channel blockers (verapamil and gallopamil) and synaptic plasma membranes (SPM) from bovine brain or human lymphocyte and platelet plasma membranes were studied. Changes in binding parameters of [3H]imipramine, [3H]desmethylimipramine and [3H]gallopamil were determined after addition of unlabelled verapamil or imipramine and after addition of phosphatidylserine (PS) (PS-stimulation). Specific binding of [3H]imipramine to SPM was decreased and [3H]desmethylimipramine binding was increased by 1 microM verapamil. [3H]gallopamil binds specifically to SPM as well as to platelet and lymphocyte membranes. [3H]gallopamil binding to SPM or lymphocyte plasma membranes was PS-stimulated in contrast to platelet plasma membranes without PS effect on binding. Imipramine inhibited both [3H]gallopamil binding and PS-stimulated [3H]gallopamil binding to SPM or lymphocyte plasma membranes. Mutual effects of tricyclic antidepressants and Ca(2+)-channel blockers on their binding sites require relatively high drug concentrations. Mechanism of Ca(2+)-channel blockers action in the treatment of depression may be connected rather with changes in signal transduction through serotonin and catecholamine receptor systems than with direct interaction of drugs with binding sites for tricyclic antidepressants.
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PMID:[Ca(2+)-channel blockers and binding of tricyclic antidepressive agents]. 755 47

The effect of chronic mild stress (CMS) and chronic treatment with the tricyclic antidepressant drug imipramine (10 mg/kg/day for 5 weeks) on neuronal responsiveness to the alpha 1-noradrenergic agonist phenylephrine and serotonin (5-HT) was examined ex vivo, in the CA1 cell layer of the rat hippocampal slice preparation. We corroborated some previous findings that CMS, which had been used as an animal model of depression, decreased the consumption of a 1% sucrose solution and that that effect was reversed by chronic administration of imipramine. Imipramine did not change the sucrose consumption in control animals. In both control and stressed animals, phenylephrine (5 microM) and 5-HT (10 microM) attenuated the amplitude of the population spikes evoked in the CA1 pyramidal cell layer by stimulation of Schaffer collateral/commissural fibers. Those inhibitory effects of phenylephrine and 5-HT were significantly potentiated by chronic treatment with imipramine. The imipramine-induced potentiation was similar in slices from control and stressed animals. These results suggest that the imipramine-induced functional changes in alpha 1-noradrenergic and serotonergic receptors in the hippocampus are not involved in the anti-anhedonic effect of chronic imipramine administration in the CMS model of depression.
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PMID:The effect of chronic treatment with imipramine on the responsiveness of hippocampal CA1 neurons to phenylephrine and serotonin in a chronic mild stress model of depression. 761

At the Drug Detoxification, Rehabilitation, and Aftercare Program of the Haight-Ashbury Free Clinics, we conducted a double-blind, controlled, randomized clinical trial of imipramine in the treatment of cocaine and methamphetamine abusers. The purpose of the trial was to test the efficacy of imipramine as a treatment for stimulant dependence and to establish the feasibility of conducting a controlled clinical trial at the clinic under conditions that approximated usual clinical practice. Subjects were randomly assigned to receive either 10 or 150 mg/day of imipramine. Imipramine 10 mg/day was the control condition. Subjects could receive study medication for up to 180 days. One-hundred eighty-three subjects participated in the study: 151 were cocaine dependent and 32 were methamphetamine dependent. In addition to receiving study medication, all subjects were assigned to intensive drug abuse counseling, which included an HIV education component. Using an intention-to-treat analysis, we found that retention in treatment was significantly longer for subjects who were treated with 150 mg of imipramine compared to control. However, we found no consistent differences between the two groups of subjects in Beck Depression Inventory scores, stimulant craving, self-report of time since last use of stimulants, or percent of urinalyses positive for stimulants. The feasibility of conducting a controlled, randomized clinical trial of medication for treatment of drug abuse was established for this community clinic setting.
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PMID:Imipramine for the treatment of cocaine and methamphetamine dependence. 773 70

Long-term treatment of depression encompasses two separate phases: relapse and recurrence prevention. Relapse prevention aims to consolidate the response to acute treatment. Some tricyclic antidepressants (TCAs) have been shown to be effective, possibly in lower than standard acute treatment doses. The selective serotonin reuptake inhibitors (SSRIs) have been shown to be effective at the same minimum effective doses used to treat acute depression, or in a lower dose as with citalopram. Recurrence prevention aims to reduce the risk of onset of a new episode of depression in patients with recurrent depression. Imipramine has been thoroughly studied in unipolar depressed patients in full therapeutic doses for up to five years and is clearly effective. Other TCAs have not been adequately tested and may not all be equally effective. The SSRIs fluoxetine, paroxetine and sertraline have also been shown to be effective in reducing the risk of new episodes of depression.
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PMID:Long-term treatment of depression. 787 35


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