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Cocaine abuse may lead to overdose (related to seizures and/or status epilepticus) and to diseases (schizophrenia, depression, and anxiety). This work was designed to study the influence of drugs used to treat psychopathologies associated with cocaine abuse on cocaine-induced seizures and mortality in mice. Fluoxetine (10, 20, 40 mg/kg), imipramine and buspirone (5, 10 mg/kg), pimozide (10, 20 mg/kg), lithium (56.3, 112.5 mg/kg), and naltrexone (25, 50 mg/kg) were administered intraperitoneally, 30 minutes prior to cocaine (90 mg/kg, ip). The animals were observed (30 minutes) to determine: latency to first seizure, number of seizures, and number of deaths after cocaine overdose. Fluoxetine, imipramine, buspirone, and pimozide had pro- or anticonvulsant effects depending on the dose. Smaller doses protected and higher doses increased cocaine-induced seizures and/or mortality. Naltrexone worsened and lithium protected against seizures. Thus, these results suggest that caution should be taken in the selection of pharmacotherapy and dosages for patients with cocaine addiction because of the possibility of potentiating cocaine toxicity.
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An antidepressant drug, imipramine, given chronically increased the social interaction between rats. A neuropeptide, vasopressin, demonstrated a similar, although weaker effect.
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The role of the serotonin receptor 4 (5-HT4R) pathway in cardiac excitation-contraction coupling (ECC) remains unclear. In the brain, induction of the calcium (Ca(2+))-binding protein p11 enhances 5-HT4R translocation and signaling and could therefore be considered as a modulator of the 5-HT4R pathway in the myocardium. p11 expression is increased by brain-derived neurotrophic factor (BDNF) or antidepressant drugs (imipramine). Thus, we investigated whether p11 regulates the 5-HT4R pathway in the heart in physiological conditions or under pharmacological induction and the effects on calcium handling.
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The catalytic activity of cytochrome P450 enzymes is known to be affected by presence of organic solvents in in vitro assays. However, these effects tend to be variable and depend on the substrate and CYP450 isoform in question. In the present study, we have investigated effect of ten water miscible organic solvents (methanol, ethanol, propanol, isopropanol, acetone, acetonitrile, dimethylsulphoxide, dimethylformamide, dioxane and PEG400) on water soluble substrates of CYP450, metoprolol and imipramine, at 0, 0.1, 0.25, 0.5, 0.75 and 1% v/v concentration in rat liver microsomes. Organic solvents studied had a concentration dependent inhibitory effect on the metoprolol and imipramine metabolism activity. Metoprolol metabolism was found to be more susceptible to the organic solvents, almost all the ten solvents had more or less inhibitory effect compared to imipramine metabolism. Except acetone, PEG400 and dimethylsulphoxide, all solvents had ~50% inhibition of total metoprolol metabolism activity, while in case of imipramine metabolism activity, only n-propanol, isopropanol and PEG400 had ~50% inhibition at 1% v/v. Interestingly, methanol, dimethylsulphoxide and acetonitrile had negligible effect on the imipramine metabolism (less than 10% inhibition at 1% v/v) while, total metoprolol metabolism activity was substantially inhibited by these solvents (MeOH 52%, DMSO 29% and ACN 47% at 1% v/v). In both cases, dioxane was found to be the most inhibitory solvent (~90% inhibition at 1% v/v).
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Although there are controversial issues (the "American view" and the "European view") regarding the construct and definition of agoraphobia (AG), this syndrome is well recognized and it is a burden in the lives of millions of people worldwide. To better clarify the role of drug therapy in AG, the authors summarized and discussed recent evidence on pharmacological treatments, based on clinical trials available from 2000, with the aim of highlighting pharmacotherapies that may improve this complex syndrome.
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There is increasing evidence suggesting that depression is associated with a certain degree of cognitive dysfunction. However, there is still debate on whether this dysfunction is only substantially associated with the most severe forms of depression, on whether or not it decreases in parallel with clinical response, and on the role played in these changes by psychotropic medications. In order to clarify these questions, we analyzed the performance in several cognitive tasks that involved attention and working memory of 40 untreated subjects with a diagnosis of dysthymia or major depressive disorder without melancholia. The protocol used included three audioverbal tasks: vocal reaction time (VRT), inverse spelling (IS) and text repetition (TR). The protocol was also administered to 20 healthy volunteers that were used as a comparison group. The same battery of assessments was administered 2 months later to all 60 subjects. At the time of the second assessment, patients (but not healthy volunteers) were on antidepressant medication, in accordance with common clinical practice. The authors found a longer VRT in patients versus healthy volunteers at baseline. VRT did not decrease in patients that responded to treatment. However, there was an improvement in VRT in patients that took sertraline (n=16) compared to subjects taking imipramine (n=11). This fact was not attributable to differences in antidepressant response. Performance in the two other tasks was globally worse in the patient group than in the comparison group, and there was also an absence of improvement in the scores of patients who responded to treatment. However, when the sample was stratified by illness duration, individuals with less than 10 years from the first episode of depression showed a decrease in IS errors compared to the healthy volunteers. It is concluded that patients with nonmelancholic depression suffer from cognitive dysfunction, that this dysfunction persists after clinical improvement and that at least attention is influenced by the type of medication taken. Time from onset of the disorder also seems to influence changes in cognitive performance.
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Uptake of serotonin and [3H]imipramine binding were studied in parallel in the platelets of control, depressed and schizophrenic patients. In the depressed patient group, uptake of serotonin was consistently reduced while [3H]imipramine binding was only decreased in a number of these patients. In the schizophrenic group, uptake of serotonin was reduced to 62% of control with no changes in [3H]imipramine binding being observed. These data demonstrate a clear dissociation between uptake of serotonin and [3H]imipramine binding sites in human platelets. The possible functional role of these [3H]imipramine binding sites remains to be determined.
A tricyclic antidepressant, C-labeled imipramine was synthesized by N-methylation of desipramine with 11CH3I to assist in the imaging of the human imipramine receptor by positron emission tomography. The radiochemical yield after purification of 11C-imipramine by high performance liquid chromatography was 28-63% at a specific activity of 26-53 Ci/mmol. The time required for synthesis, including purification was 30 min from the end of 11CH3I trapping. The organ distribution of 11C-imipramine was investigated in mice at various times after i.v. injection. The main accumulation of radioactivity was in the kidney, followed by the lung and the heart. In the brain, the radioactivity levels in the hypothalamus and striatum were the highest and remained constant, differentiating them from other portions of the brain. Furthermore, the result of a binding assay with 3H-labeled imipramine suggested that the regional distribution of 11C-imipramine in the same mouse brain correlated to that of the high affinity imipramine binding site.
The biochemical mechanism of action produced by a new antidepressant pyrazidol (1,10-trimethylene-8-methyl-1, 2, 3, 4-tetrahydropyrazino[1,2-a] indole hydrochloride) includes the inhibitory influence on the neuronal uptake of norepinephrine and a reversible comparatively short-lived inhibitory effect on the MAO activity.
Dopamine (DA) receptor sensitivity to apomorphine (APO) was assessed in the rat nigrostriatal system following chronic antidepressant treatment. Imipramine (IMI), iprindole (IPR) or vehicle was administered to rats for 10 days (10 mg/kg i.p., b.i.d.). Two and a half days after the last injection 3,4-dihydroxyphenylacetic acid (DOPAC) levels were measured in rat striata following injection of APO (50 or 100 micrograms/kg s.c.) or vehicle. In contrast with rats receiving chronic vehicle injections, rats chronically treated with IMI or IPR failed to exhibit a significant APO-induced fall in striatal DOPAC levels. Antidepressant-treated animals, however, exhibited significantly lower basal DOPAC levels than vehicle-treated rats. In an effort to localize the diminished APO response, DA autoreceptor sensitivity to APO was assessed in drug- and vehicle-treated animals. Employing gamma-butyrolactone (GBL) and a dihydroxyphenylalanine (DOPA) decarboxylase inhibitor to elevate striatal DOPA, the APO-induced reversal of DOPA elevation was used as an index of DA autoreceptor sensitivity. This GBL-stimulated in vivo tyrosine hydroxylation was similarly reversed by APO (125, 250 or 500 micrograms/kg i.p.) in IMI-, IPR- and vehicle-treated animals. In view of these findings, we propose that the blunted biochemical response to APO observed in animals pretreated with antidepressants does not originate as a result of alterations in the sensitivity of DA autoreceptors located on the striatal presynaptic nerve terminal.
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Electrogenic H(+)-ATPase was found in neurosecretory granules from bovine posterior pituitary. This enzyme was sensitive to bafilomycin, a specific inhibitor of vacuolar H(+)-ATPase, and was inactivated completely by cold treatment in the presence of MgATP and NaNO3. Immunoblot analysis showed the presence of immunologically identical polypeptides (72, 57, and 34 kDa) in the ATPases of the neurosecretory granules and chromaffin granules. The granules showed MgATP-dependent activity for 5-hydroxytryptamine (serotonin) uptake. This uptake was temperature-dependent and showed saturation kinetics (apparent Km for 5-hydroxytryptamine, 2 microM) and counter-flow. Reserpine and tetrabenazine at 1 microM inhibited the uptake, whereas imipramine at 2 microM had no effect. Dopamine, epinephrine and norepinephrine were also inhibitory. The uptake was abolished by various treatments that dissipated the electrochemical H+ gradient or inhibited the H(+)-ATPase. These results indicate that a vacuolar type H(+)-ATPase in the neurosecretory granules forms an electrochemical H+ gradient that drives 5-hydroxytryptamine uptake by a specific transport system. A similar granular fraction from the anterior pituitary had no ATP-dependent activity for 5-hydroxytryptamine uptake.
To describe a middle-aged patient with Charles Bonnet syndrome (CBS) suffering from concurrent major depression.
To explore the hypothesis that depressed patients with low pretreatment levels of urinary 3-methoxy-4-hydroxyphenylglycol (MHPG) respond more favorably to antidepressant drugs which act on noradrenergic neuronal systems than do patients with high MHPG levels, the authors administered 150--200 mg/day of imipramine or maprotiline to 13 depressed patients. All of the 5 patients with low pretreatment MHPG levels responded to treatment compared with 1 of the 14 patients with high MHPG levels; 4 patients dropped out of the study.
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The purpose of this study was to investigate the effects of two lipidosis-inducing drugs (the anorectic drug chlorphentermine and the tricyclic antidepressant-imipramine) upon the estrous cycle of rats and upon the morphology of the vaginal and uterine epithelia. After two weeks of continuous administration of high daily drug doses, the estrous cycle became stagnant. Ultrastructurally, the vaginal and uterine epithelia contained storage lysosomes which were filled with undigested polar lipids appearing as multilamellated material. The uterine luminal epithelium was most severely affected. The estrous cycle was abolished also by treatment with the anorexigenic drug phentermine, although this compound does not cause lipidosis. Therefore, the cessation of the estrous cycle cannot be attributed to the lipidosis as induced by chlorphentermine and imipramine; probably it is a consequence of the main actions of these psychotropic drugs. The biological basis for the exceedingly severe lipidosis in the uterine luminal epithelium is suggested to be the heavy load of polar lipids physiologically delivered to the lysosomal apparatus as long as the cycle-dependent apoptotic and autophagic processes were going on during the early period of drug treatment.
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Young male Sprague-Dawley rats were allocated to two placebo (restraint and sham transcranial magnetic stimulation), one active control (imipramine), and four transcranial magnetic stimulation groups at 1, 5, 15 and 25 Hz and 1000 stimuli each. The Porsolt Swim Test was performed on day 1 (experiment 1). In an extension (experiment 2), the treatments were repeated on days 2 through 5, and the Swim Test repeated on days 3, 5, and 7.