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The effect of fluvoxamine, a selective serotonin (5-HT) reuptake inhibitor, was studied in a model of anxiety and/or obsessive compulsive disorder (OCD) in mice. In the anxiety/OCD model, marble-burying behavior, marble-burying was significantly suppressed by fluvoxamine at 30 and 60 mg/kg, p.o. and the monoamine reuptake inhibitor clomipramine, at 60 mg/kg, p.o. No suppressive effect, however, was observed by the selective norepinephrine reuptake inhibitor desipramine at doses from 15 to 60 mg/kg, p.o. Suppressive effects were obtained by the serotonergic anxiolytic buspirone at 30 and 60 mg/kg, p.o. and the benzodiazepine anxiolytic diazepam at 10 mg/kg, p.o. The effect of fluvoxamine on marble-burying was slightly attenuated after repeated administration. On the other hand, both the effects of buspirone and diazepam completely disappeared after repeated administration. Effect of fluvoxamine on the marble-burying was unaffected by the 5-HT2 antagonist ritanserin. However, the 5-HT1A antagonist NAN-190 (1-(2-methoxyphenyl)-4-[4-(2-phthalimido)butyl] piperazine) inhibited the suppressive effect of fluvoxamine on the marble-burying. From these results, the 5-HT1A-receptor subtype may be involved in the suppressive effect of fluvoxamine on the marble-burying, but the 5-HT2-receptor subtype is not involved in this effect.
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Headache was classified, in conformity to the classification of headache as specified by the Ad Hoc Committee, into migraine, contraction and combined types and others. Tricyclic antidepressant clomipramine having pharmacological properties, which are said to relatively and uniquely inhibit the reuptake of serotonin in the synapses, was administered for headaches and the clinical effects on headaches were examined. Headaches assumed to be attributable to depression were excluded by means of quationing and Zung's self-rating depression scale. Furthermore, the MMPI, MPI and MAS mentality tests were also employed to clarify the characters and traits of these patients with headache. Also, the biochemical mechanism playing a part in the occurrence of headache was conjectured from the pharmacological action pattern of the antidepressant.
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The objective of the study was to analyze characteristics of SS French pharmacovigilance reports, especially involved drugs and nature of drug-drug interactions (DDIs).
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The effect of citalopram, a selective serotonin reuptake inhibitor (SSRI) antidepressant, was studied on cardiac action potential configuration and compared with that of the tricyclic antidepressant (TCA) clomipramine. Conventional microelectrode techniques were used in right ventricular papillary muscle preparations of the guinea pig. Citalopram caused a concentration-dependent (10-100 microM) shortening of action potential duration (APD), depression of plateau and overshoot potential, and reduction of maximum velocity of depolarization (V(max)). No significant changes in resting membrane potential were observed. Similar results were obtained with clomipramine; however, reduction of V(max) and overshoot was more pronounced with clomipramine, whereas citalopram caused relatively greater shortening of APD. Effects of both drugs were partly reversible. The results indicate that the SSRI antidepressant citalopram, similarly to TCA compounds, alters cardiac action potential configuration in guinea pig ventricular muscle, probably owing to inhibition of cardiac Na(+) and Ca(2+) channels. Differences in cardiac side effects of the two drugs may be related to their different actions on cardiac action potential configuration.
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Uptake of [3H]clonidine was linear for up to 2 min, Na+-independent, and insensitive to changes in membrane potential, but strongly H+-dependent. The uptake rate of clonidine was saturable with kinetic parameters of 0.5+/-0.1 mM (Kt) and 16.6+/-1.8 nmol/2 min per mg of protein (Vmax) at an outside pH of 7.5. Many drugs such as clonidine, guanabenz, methamphetamine, imipramine, clomipramine, nortriptyline, quinine, xylazine, ephedrine, and diphenhydramine strongly inhibited the [3H]clonidine uptake with Ki values between 0.15 and 1 mM.
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The objective of this study was to evaluate the efficacy and tolerability of citalopram in the long-term treatment of adult outpatients with panic disorder with or without agoraphobia.
50 so-called therapy-resistant depressed inpatients have been treated with daily i.v. infusions of Clomipramine in a high dosage, using a fixed therapy schedule with increasing and decreasing dosage ranging from 250 to 500 mg. The majority of the inpatients showed sufficient or good therapeutic effects, notable side effects were rare. The therapeutic possibilities of so-called therapy-resistant depressions are discussed.
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Data were organized according to the pharmacologic agent used in the management of SSRI dysfunction, target population, SSRI implicated, type of sexual dysfunction, experimental design, and treatment response. Data were extracted from methodology and results sections of reports. Methodologic flaws included failure to account for gender differences, omission of SSRI dose and duration, and use of concomitant drugs.
25 patients with therapy-resistant depressive syndromes of various origins were treated by the infusion of high Hydiphen doses, a very effective thymoleptic drug with no dissociation between its drive increasing and spirit raising actions. The results yielded by this treatment varied from good to very good in respect of endogenic depressions, in which the mood was observed to change at doses between 150 and 425 mg/d, depending on the severity of the depression. The results of this treatment were less satisfactory in the case of reactive and bran-organically induced depressions.
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SRG is of therapeutic value for depression-like disorders, and antioxidation may be one of the mechanisms underlying its antidepressant action.
Stimulant medication improves hyperactivity, inattention, and impulsivity in both pediatric and adult populations with Attention Deficit Hyperactivity Disorder (ADHD). However, data regarding the optimal dosage in adults is still limited.
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Obsessive-compulsive disorder (OCD) has been successfully treated with proserotonergic agents for some years. Clomipramine was the first drug used, but several clinical trials have been conducted more recently to assess the antiobsessional efficacy of selective serotonin reuptake inhibitors (SSRIs). The aim of this study was to compare the antiobsessional efficacy of three SSRIs, fluvoxamine, paroxetine, and citalopram. Thirty obsessive-compulsive patients without comorbid axis I diagnoses except for tic disorder as assessed by DSM-III-R criteria gave informed consent and were recruited consecutively; they underwent a 10-week randomized treatment with fluvoxamine, paroxetine, or citalopram. Ratings were performed under blind conditions every 2 weeks from baseline to the end of the study and by the Yale-Brown Obsessive-Compulsive Scale, the National Institute of Mental Health-Obsessive-Compulsive Scale, the Clinical Global Impressions Scale, and the Hamilton Rating Scale for Depression. Quantitative and qualitative analyses of the antiobsessional efficacy of the three drugs were completed with analysis of variance with repeated measures and survival analysis. The results showed no significant differences between the three treatments. The preliminary conclusions drawn from this study concern the interchangeable antiobsessional effects of different SSRIs, although further studies of "cross-response" to these drugs are needed.
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1. The appearance of Fm theta, the distinct EEG theta rhythm in the frontal midline area during performance of a mental task, reflects relief from anxiety in humans. 2. In the present study, the anxiolytic effects of low-dose clomipramine were examined by monitoring the Fm theta amount, the STAI scores and the plasma 5-HIAA concentration in 24 male university students with (Fm theta group, n = 12) and without (non-Fm theta group, n = 12) Fm theta. 3. Subjects were given placebo, 10 mg and 30 mg clomipramine in a double-blind crossover design. Blood samples were obtained, STAI scores were determined, and EEGs were recorded before and during the performance of an arithmetic addition task. The test was repeated twice: before and 3 hrs after drug administration. 4. In the non-Fm theta group, 10 mg clomipramine decreased the 5-HIAA concentration and state anxiety scores but increased the Fm theta amount, while 30 mg clomipramine slightly increased only the Fm theta amount. However, there were no differences in these items before and after clomipramine administration in the Fm theta group. 5. These results suggest that low doses of clomipramine such as 10 mg may exert anxiolytic effects during the acute phase of treatment in highly anxious humans.
The glucocorticoid receptor (GR) is a key regulator of the hypothalamic-pituitary-adrenal (HPA) axis. Mood disorder patients often exhibit abnormalities in this axis. Although the clinical benefit of antidepressants is associated with the normalization of the disturbed HPA activity by enhanced negative feedback of the HPA axis, the precise mechanism remains unknown. In order to examine the effect of antidepressants on the translocation of GR into the nucleus, we performed time-lapse observation on SY5Y cells that had been transiently transfected with plasmids expressing the green fluorescence protein (GFP)-tagged GRalpha. Clomipramine and desipramine facilitated dexamethasone (Dex)-induced GFP-GRalpha nuclear translocation. Coincubation of verapamil, an inhibitor of membrane steroid transporters, showed little or no additive effect on GFP-GRalpha nuclear translocation induced by both Dex and clomipramine. In the absence of Dex, antidepressants did not induce the translocation of GFP-GRalpha into the nucleus. Using real-time PCR, we examined the effect of antidepressants on splicing isoform of GR, GRalpha, and GRbeta in SY5Y and Jurkat cells. Incubation with paroxetine and desipramine for 48 h and 7 days increased GRalpha expression, whereas the expression of GRbeta remained stable. Antidepressants did not alter the expression of SRp30c that is associated with alternative splicing of GR transcript. Thus, antidepressants exert differential effects on the translocation and expression of GR to enhance GR signaling.
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228 physicians (86%) who answered the questionnaire.
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Abnormalities in serum cholesterol levels of patients with mood disorders have been identified in epidemiological studies. However, evidence for an influence of dietary cholesterol on behavioral models is poor. Here, we investigated the behavioral changes of Wistar male rats fed a 2% cholesterol-enriched diet for 2 months in experimental models of depression and anxiety, such as the forced swim test (FST) paradigm and the novelty-induced grooming sampling test (NGT). The correlation between behavioral depression and impaired cognitive capacity was also examined testing rats in the Morris water maze (MWM) task one day after the FST. Different groups of rats fed various dietary regimens, were subjected to acute or repeated treatment (14 days) with clomipramine hydrochloride (50 or 25 mg/kg), diazepam (1 mg/kg) or with the peripheral benzodiazepine receptors (PBRs) antagonist, isoquinoline PK11195 (1 mg/kg) injected intraperitoneally (i.p.). Rats fed the cholesterol-enriched diet showed a significant decrease of grooming score in the NGT and of immobility time in the FST in comparison to animals fed a standard diet. Furthermore, the anxiolytic and antidepressant effects of diazepam and clomipramine were not affected by the different diets. Only after repeated treatment, PK11195 impaired the performance of animals fed a standard diet in the FST, and exhibited an anxiolytic-like profile in animals fed either the cholesterol-enriched or the standard diet. The improved performance in the FST was followed by a better learning performance in the acquisition phase of the MWM. These results suggest that effects of cholesterol-enriched diet on the behavioral reaction of rats in experimental models of mild stress may involve PBRs. They deserve attention in order to clarify the clinical correlation between plasma cholesterol levels and mood disorders in humans.
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There have been an increased number of recent reports on orgasm-related sexual dysfunction coincident with selective serotonin reuptake inhibitor (SSRI) treatment. In contrast, it has also been reported that SSRIs improve sexual dysfunction. Low doses of clomipramine and paroxetine, potent 5-hydroxytryptamine reuptake blockers, have been found to retard ejaculation time. We hypothesized that the SSRI fluoxetine might be effective in treating premature ejaculation. In an 8-week open-label clinical study, 11 male patients with premature ejaculation were treated with fluoxetine. After a washout period of 2 weeks, each patient was assigned to receive fluoxetine, 20 mg/day for 2 weeks, and then titrated to 60 mg/day, depending on the patient's tolerability and clinical response. A within-subjects comparison of pre- and posttreatment intravaginal ejaculation latency time revealed a significant improvement. Fluoxetine treatment produced significant improvements in self-visual analogue scale scores for sexual desire, anxiety for rapid ejaculation, and partner's satisfaction with ejaculation and overall sexual function. These data suggest that serotonergic antidepressants may be effective in treating rapid ejaculation in men and underline the need to carry out a double-blind, placebo-controlled trial to confirm these results.
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An 11-year-old boy with asthma had been receiving a controlled release theophylline preparation. He was prescribed fluvoxamine for a depressive disorder and within a week complained of severe headaches, tiredness and vomiting. His serum theophylline concentration had increased from 14.2 mg/L (shortly before fluvoxamine was started) to 27.4 mg/L. Fluvoxamine was withdrawn and theophylline concentrations decreased. Clomipramine was substituted for fluvoxamine with no further problems, and a later theophylline concentration was 13.7 mg/L. Competitive inhibition of hepatic microsomal enzymes by fluvoxamine may have been responsible for the elevated theophylline concentrations and toxicity observed in this case.
On follow-up, 23 of the subjects (43%) still met diagnostic criteria for OCD, and only three (6%) could be considered in true remission. Thirty-eight subjects (70%) were taking psychoactive medication at the time of follow-up. Although OCD symptoms continued, the group as a whole was significantly improved at follow-up, with only 10 subjects (19%) rated as unchanged or worse. A worse OCD outcome score at follow-up was predicted in a stepwise multiple regression by (1) more severe OCD symptoms score after 5 weeks of clomipramine therapy, (2) lifetime history of a tic disorder, and (3) presence of parental Axis I psychiatric diagnosis (R2 = .31, P < .01).
Glial activation and neuroinflammatory processes play an important role in the pathogenesis of neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and HIV dementia. Activated glial cells can secrete various proinflammatory cytokines and neurotoxic mediators, which may contribute to neuronal cell death. Inhibition of glial activation may alleviate neurodegeneration under these conditions. In the present study, the antiinflammatory and neuroprotective effects of tricyclic antidepressants were investigated using cultured brain cells as a model. The results showed that clomipramine and imipramine significantly decreased the production of nitric oxide or tumor necrosis factor-alpha (TNF-alpha) in microglia and astrocyte cultures. Clomipramine and imipramine also attenuated the expression of inducible nitric oxide synthase and proinflammatory cytokines such as interleukin-1beta and TNF-alpha at mRNA levels. In addition, clomipramine and imipramine inhibited IkappaB degradation, nuclear translocation of the p65 subunit of NF-kappaB, and phosphorylation of p38 mitogen-activated protein kinase in the lipopolysaccharide-stimulated microglia cells. Moreover, clomipramine and imipramine were neuroprotective as the drugs reduced microglia-mediated neuroblastoma cell death in a microglia/neuron co-culture. Therefore, these results imply that clomipramine and imipramine have antiinflammatory and neuroprotective effects in the central nervous system by modulating glial activation.
A 44-base-pair insertion/deletion polymorphism in the promoter region of the human serotonin (5-HT) transporter (5-HTT) gene gives rise to a bi-allelic polymorphism designated long (l) and short (s). The s variant is associated with a lower expression of 5-HTT sites and a reduced efficiency of 5-HT reuptake.
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Proconvulsant effects are associated with a subgroup of psychotropic drugs. Second-generation antidepressants other than bupropion have an apparent anticonvulsant effect. Depression, psychotic disorders, and OCD are associated with reduced seizure threshold.