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Several clinical reports have documented a beneficial effect of adding atypical antipsychotic drugs to ongoing treatments with antidepressants, particularly selective serotonin reuptake inhibitors, in ameliorating drug-resistant depression. The aim of this paper was to summarize some preclinical evidence describing the mechanism responsible for the therapeutic action of combined treatment with antidepressants and atypical antipsychotics and also some clinical data supporting the efficacy and safety of the augmentation strategy for improving antidepressant-resistant depression using atypical antipsychotics. This analysis is based on five microdialysis studies and nine behavioral studies assessing the impact of combined atypical antipsychotic and antidepressant treatments on extracellular levels of dopamine, serotonin and noradrenaline in the prefrontal cortex of freely moving rats and on antidepressant-induced effects, respectively. In addition, clinical data demonstrating the efficacy and safety of augmentation strategies for treatment-resistant depression using atypical antipsychotics were included. Combined treatment of rats with all studied atypical antipsychotics (olanzapine, risperidone, clozapine and quetiapine) and antidepressants (citalopram, fluoxetine and fluvoxamine) increased the extracellular level of dopamine in the prefrontal cortex compared to a respective drug given alone; in addition, a combination of olanzapine or quetiapine plus fluoxetine or fluvoxamine increased the levels of dopamine and noradrenaline. Moreover, atypical antipsychotics administered in a low dose enhanced the antidepressant-like activity of antidepressants, with (among other mechanisms) the serotonin 5-HT1A, 5-HT2A and adrenergic α2 receptors likely playing an important role in their action. The results support the conclusion that atypical antipsychotics may be effective as adjunctive therapy in treatment-resistant depression; however, their adverse effect profile may be unfavorable in some patients.
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A 22-year-old woman was found dead in her bed, and subsequent postmortem examination was performed using ordinary methods such as external examination, Triage®, and computed tomography (CT) scan which demonstrated a high-density content of the duodenum. Autopsy and quantitative analysis of drugs present in the GI tract showed that high amounts of radiopaque psychotic agents such as fluvoxamine maleate, carbamazepine, and zolpidem tartrate had been responsible for the high-density profile of the duodenum. Postmortem quantitative analysis of drugs in the blood suggested that death had been caused by fatal intoxication with fluvoxamine maleate. Thus, postmortem CT could offer an opportunity to suspect drug intoxication due to radiopaque psychotic agents such as chloral hydrate, phenothiazine, bromovaleryl urea, fluvoxamine maleate, and probably zolpidem tartrate, although it is neither a specific nor a quantitative test for drugs. Therefore, postmortem CT happened to provide clues to investigation of drug intoxication in the present case.
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Selective serotonin-reuptake inhibitors (SSRIs) are used in the treatment of various forms of psychiatric disorders. Preclinical studies in laboratory animals have indicated that SSRIs were not genotoxic, but clear results from in vitro testing of SSRIs in a human cell system are currently scarce. The purpose of this study was to investigate whether SSRIs might be genotoxic. Sertraline was chosen as model SSRI, since it appears to be at least as well-tolerated as other SSRIs and may even have a more favourable side-effect profile. Unlike fluoxetine, fluvoxamine and paroxetine, sertraline has low potential for pharmacokinetic drug interactions. So, sertraline would be considered first in the treatment of psychiatric disorders requiring SSRI therapy in the future. We therefore examined peripheral lymphocytes from sertraline-treated patients for both sister chromatid exchanges (SCEs), cells with a high frequency of SCEs (HFC) and chromosome aberrations (CA) to evaluate the clastogenicity of SSRIs.
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Prescribing patterns for SSRIs at BC Children's Hospital are consistent with the available evidence in the pediatric population. Furthermore, with the exception of citalopram, provincial outpatient and inpatient prescriptions appear to follow published national guidelines. Hospital SSRI usage more closely reflects the available literature than outpatient community usage does.
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Conventional meta-analyses have shown inconsistent results for efficacy of second-generation antidepressants. We therefore did a multiple-treatments meta-analysis, which accounts for both direct and indirect comparisons, to assess the effects of 12 new-generation antidepressants on major depression.
With a consensus, authors (A.A.S. and S.P.) extracted and checked the data independently on the basis of predetermined exclusion and inclusion criteria. Effect size estimates were calculated using Comprehensive Meta-Analysis software.
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Biotransformation of nefazodone to its metabolic products, and of meta-chlorophenylpiperazine (mCPP) to para-hydroxy-mCPP, was studied in vitro using human liver microsomes and heterologously expressed human cytochromes. Nefazodone and metabolites were also tested as inhibitors of alprazolam hydroxylation, reflecting activity of cytochrome P450-3A isoforms.
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The mechanism by which the psychostimulant methamphetamine (METH) increases locomotor activity may be attributable to indirect activation of serotonin (5-HT) and dopamine (DA) receptors. In the present study, the ability of the serotonin reuptake inhibitor fluvoxamine, 5-HT(1A), 5-HT(1B), 5-HT(2A) and 5-HT(2C) receptor antagonists WAY100635, GR127935, M100907 and SB242084, and the 5-HT(2C) receptor agonists WAY163909 and Ro 60-0175 or the 5-HT synthesis inhibitor para-chlorophenylalanine (pCPA) to alter METH-induced hyperactivity was analysed. Further, for comparative purposes, the involvement of the DA D(1) and D(2) receptor antagonists SCH23390 and haloperidol, D(2) partial agonists terguride, (-)3PPP and aripiprazole and finally clozapine were assessed. Doses of pCPA that attenuated 5-HT levels reduced METH activity. The 5-HT(1B) antagonist GR127935 had no effect on METH-induced locomotor activity but blocked that induced by MDMA. The 5-HT(1A) antagonist WAY100635 reduced activity but this did not reach significance. In contrast, M100907 (minimal effective dose; MED=0.125 mg/kg), WAY163909 (MED=3mg/kg), Ro 60-0175 (MED=3mg/kg), haloperidol (MED=0.1mg/kg), clozapine (MED=5mg/kg), aripiprazole (MED=1mg/kg), (-)3PPP (MED=3mg/kg), terguride (MED=0.2mg/kg) and SCH23390 (MED=0.001325 mg/kg) attenuated METH-induced locomotor activity. Administration of 20mg/kg fluvoxamine attenuated, while SB242084 (MED=0.25mg/kg) potentiated METH-induced activity. These results contribute significantly to the understanding of the mechanism of action of this psychostimulant and suggest for the first time, that METH-induced locomotor stimulation is modulated by 5-HT(2A) and 5-HT(2C) receptors, but demonstrate that 5-HT(1B) receptors are not directly involved. The involvement of the dopaminergic system was also demonstrated.
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The administration of fluvoxamine to patients with depressive state after cerebral infarction alleviated both the depressive state and sleep disturbances. Increased melatonin levels by the administration of fluvoxamine may contribute to improvement in sleep disturbance, one of the major symptoms of depression.
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It has been suggested that treatment with selective serotonin reuptake inhibitors (SSRIs) in combination with pindolol, a partial agonist at the 5-HT(1A) receptor, may produce a fast antidepressant response. However, inconsistent results have been obtained in clinical studies with combination of the two drugs. Some studies, most using paroxetine, show an acceleration of the antidepressant response, whereas studies with other SSRIs find no marked latency reduction.
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Fluvoxamine, a selective serotonin reuptake inhibitor, was investigated in a 6-week double-blind study among severely ill inpatients with DSM-III major depression. All but 1 patient also fulfilled criteria for melancholia. Following a 3-day placebo wash-out patients were randomly assigned to fluvoxamine, imipramine or placebo. Sixty of 81 patients completed at least 2 weeks following wash-out and were evaluated for efficacy. Analysis of covariance (controlling for baseline scores) showed significant (p less than 0.05) differences on CGI severity and BPRS total and a similar trend (p = 0.08) on the Hamilton Depression Scale. Fluvoxamine was superior (p less than or equal to 0.02) to both placebo and imipramine on these measures. Fluvoxamine's most common adverse effects were nausea and agitation. The number of fluvoxamine patients withdrawn for side-effects was less than imipramine and not significantly different than placebo. Fluvoxamine was not associated with significant changes in vital signs, ECG or laboratory tests. The results therefore indicate that fluvoxamine is a safe and highly effective treatment for hospitalized patients with major depression.
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Plasma interleukin-1 beta (Il-1 beta) interleukin-6 (Il-6) and tumor necrosis factor-alpha (TNF-alpha) concentrations were measured in 26 women with Anorexia Nervosa (AN), nine of the restricted type (AN-R) and 17 of the binge-eating/purging type (AN-BP), in 24 women with Bulimia Nervosa (BN) and in 26 healthy age- and sex-matched controls. Concentrations of the cytokines were measured at the beginning of the study before starting any treatment and then after 1 and 3 months of combined cognitive-behavioral and pharmacological therapy (fluoxetine for AN-R and AN-BP, amineptine for AN-BP and BN, and fluvoxamine for BN). Basal values of Il-1 beta, Il-6 and TNF-alpha, were the same in patients and controls and did not change during treatments, in spite of the improvement of the mental disorders. This seems to exclude the possibility that alterations of basal plasma cytokine secretion are involved in the etiopathogenesis of AN and BN.
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Even a low dose of fluvoxamine increased omeprazole exposure in EMs, but did not increase omeprazole exposure in PMs after a single oral dose of omeprazole. These findings confirm a potent inhibitory effect of fluvoxamine on CYP2C19 activity. The bioavailability of omeprazole might, to some extent, be increased through inhibition of P-glycoprotein during fluvoxamine treatment.
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Fast cyclic voltammetry (FCV) at carbon fibre microelectrodes was used to monitor 'real time' endogenous noradrenaline (NA) efflux in superfused slices of rat locus coeruleus (LC) following local electrical stimulation. When stimulated with a standard train (30 pulses, 100 Hz, 0.2 ms, 10 mA, every 5 min), efflux of monoamine was constant over the experimental period (2.5 h): Amine efflux declined by only 16 +/- 5% while uptake half-life lengthened by only 9 +/- 8%. When calibrated in solutions of NA, peak amine efflux corresponded to 0.31 +/- 0.04 microM (mean +/- S.E.M., n = 28) and was removed by uptake with a half-life of 2.93 +/- 0.28 s (n = 16). The released compound was confirmed as NA on the basis of pharmacological and electrochemical criteria. Stimulated monoamine efflux was reversibly reduced by 78% by omission of Ca2+ from the superfusate for 30 min (P < 0.05). Ro 4-1284 (1 microM), a fast-acting reserpine-like drug, decreased amine efflux by 86% (P < 0.05). The monoamine oxidase inhibitor pargyline (2 microM) increased efflux by 30% (P < 0.05). Desipramine (0.05 microM), a selective NA uptake blocker, significantly increased amine efflux (by 96%, P < 0.05) and uptake half-life (by 314%, P < 0.05). Fluvoxamine (0.5 microM), the selective serotonin (5HT) uptake blocker, increased efflux by 59% (P < 0.05) and the uptake half-life by 122% (P < 0.05). Vanoxerine (GBR 12909: 0.3 microM), the dopamine (DA) uptake blocker, had no effect on amine efflux or uptake half-life. The voltammogram of the released amine had single oxidation and reduction peaks.(ABSTRACT TRUNCATED AT 250 WORDS)
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A series of double-blind hospital based studies comparing fluvoxamine with other antidepressants in depressed patients is reviewed. Overall there were no significant differences in terms of efficacy between fluvoxamine and the comparators (amitriptyline, dothiepin, lofepramine and mianserin). Fluvoxamine was shown to be associated with a low incidence of anticholinergic, cardiovascular or sedative effects. This profile of activity, together with low toxicity in overdosage, has established the place of fluvoxamine in the treatment of depressive illness.
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Mechanisms of renal ischemia-reperfusion injury remain unresolved, and effective therapies are lacking. We previously showed that dehydroepiandrosterone protects against renal ischemia-reperfusion injury in male rats. Here, we investigated the potential role of σ1-receptor activation in mediating this protection. In rats, pretreatment with either dehydroepiandrosterone or fluvoxamine, a high-affinity σ1-receptor agonist, improved survival, renal function and structure, and the inflammatory response after sublethal renal ischemia-reperfusion injury. In human proximal tubular epithelial cells, stimulation by fluvoxamine or oxidative stress caused the σ1-receptor to translocate from the endoplasmic reticulum to the cytosol and nucleus. Fluvoxamine stimulation in these cells also activated nitric oxide production that was blocked by σ1-receptor knockdown or Akt inhibition. Similarly, in the postischemic rat kidney, σ1-receptor activation by fluvoxamine triggered the Akt-nitric oxide synthase signaling pathway, resulting in time- and isoform-specific endothelial and neuronal nitric oxide synthase activation and nitric oxide production. Concurrently, intravital two-photon imaging revealed prompt peritubular vasodilation after fluvoxamine treatment, which was blocked by the σ1-receptor antagonist or various nitric oxide synthase blockers. In conclusion, in this rat model of ischemia-reperfusion injury, σ1-receptor agonists improved postischemic survival and renal function via activation of Akt-mediated nitric oxide signaling in the kidney. Thus, σ1-receptor activation might provide a therapeutic option for renoprotective therapy.
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The most favourable pharmacological treatment in terms of remission was escitalopram with an 8- to 12-week probability of remission of 0.47. Despite a high acquisition cost, this clinical effectiveness translated into escitalopram being both more effective and having a lower total cost than all other comparators from a societal perspective. From a healthcare perspective, the cost per QALY of escitalopram was €3732 compared with venlafaxine.
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A recent study suggested that selective serotonin reuptake inhibitors were inactive in 40-week-old male mice in the mouse forced swimming test, possibly because of alteration of 5-HT1 receptors.
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Three antidepressant drugs, amitriptyline as a dual-action, nonselective inhibitor of noradrenaline and a serotonin reuptake inhibitor, fluvoxamine as a selective serotonin reuptake inhibitor and maprotiline as a selective noradrenaline reuptake inhibitor, were selected, and the effect of glibenclamide on their antinociceptive activities was assessed in male Swiss mice (25-30 g) using a formalin test.
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We have compared the effects of single oral doses of fluvoxamine (50 mg and 100 mg), amitriptyline (50 mg and 100 mg), and placebo on some autonomic functions in ten healthy volunteers, using a balanced, double-blind, crossover design. Amitriptyline significantly reduced salivation, the miosis evoked by locally applied pilocarpine, and the sweat secretion evoked by locally applied carbachol. Fluvoxamine also significantly attenuated carbachol-evoked sweat gland activity, although to a smaller degree than amitriptyline; fluvoxamine did not significantly alter salivation or pilocarpine-evoked miosis. Neither treatment significantly altered the miotic responses evoked by brief light stimuli. Heart rate and blood pressure were not greatly affected by either treatment, although the fall in heart rate (erect posture) with placebo was significantly reduced by amitriptyline (100 mg). The results suggest that fluvoxamine has some anti-muscarinic activity in man, but is considerably less potent in this respect than amitriptyline.
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Seven RCTs with a total of 271 participants were included. Four SSRIs were evaluated: fluoxetine (two studies), fluvoxamine (two studies), fenfluramine (two studies) and citalopram (one study). Five studies included only children and two studies included only adults. Varying inclusion criteria were used with regard to diagnostic criteria and intelligence of participants. Seventeen different outcome measures were reported. Although more than one study reported data for Clinical Global Impression (CGI) and obsessive-compulsive behaviour (OCB), different tool types or components of these outcomes were used in each study. As such, data were unsuitable for meta-analysis. One large, high quality study in children showed no evidence of positive effect of citalopram. Two small studies in adults showed positive outcomes for CGI and OCB; one study showed improvements in aggression and another in anxiety.
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Some doses of fluvoxamine can decrease ethanol-maintained behavior more than food-maintained behavior. This might be explained by differences in reinforcement magnitude. In a previous study, the effects of fluvoxamine on fixed-ratio responding did not depend upon reinforcement magnitude. Response rates, however, differed with reinforcement magnitude. These differences in response rates might explain the failure to observe differences in the potency of fluvoxamine with changes in reinforcement magnitude. In this study, we examined whether the effects of fluvoxamine and desipramine depended on the reinforcement magnitude and response rate, by administering these drugs to pigeons responding under a multiple fixed-interval schedule, in which responding in three components was maintained by differing durations of food presentation (2, 4, and 8 s). The effects of fluvoxamine and desipramine depended jointly on control rate, reinforcement magnitude, and dose. Low fluvoxamine doses had rate-dependent effects in all three components, increasing lower rates more than higher rates: as dose increased, these rate-dependent effects became greater in the components maintained by the 2-s or 4-s food presentation; whereas, in the component maintained by the 8-s presentations, they declined. Low desipramine doses had rate-dependent effects only in the component maintained by the 2-s presentations, whereas higher doses had rate-dependent effects in components maintained by 2-s or 4-s presentations. Still higher doses had rate-dependent effects in all the three components. Although the effects of fluvoxamine and desipramine might not depend on reinforcement magnitude when studied under fixed-ratio schedules, reinforcement magnitude can modulate their effects when they are studied over a wider range of control response rates.
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We monitored real-time in vivo levels of serotonin release in the digestive system of intact zebrafish embryos during early development (5 days postfertilization, dpf) using differential pulse voltammetry with implanted carbon fiber microelectrodes modified with carbon nanotubes dispersed in nafion. A detection limit of 1 nM, a linear range between 5 and 200 nM, and a sensitivity of 83.65 nA x microM(-1) were recorded. The microelectrodes were implanted at various locations in the intestine of zebrafish embryos. Serotonin levels of up to 29.9 (+/-1.13) nM were measured in vivo in normal physiological conditions. Measurements were performed in intact live embryos without additional perturbation beyond electrode insertion. The sensor was able to quantify pharmacological alterations in serotonin release and provide the longitudinal distribution of this neurotransmitter along the intestine with high spatial resolution. In the presence of fluvoxamine, a selective serotonin reuptake inhibitor (SSRI), concentrations of 54.1 (+/-1.05) nM were recorded while in the presence of p-chloro-phenylalanine (PCPA), a tryptophan hydroxylase inhibitor, the serotonin levels decreased to 7.2 (+/-0.45) nM. The variation of serotonin levels was correlated with immunohistochemical analysis. We have demonstrated the first use of electrochemical microsensors for in vivo monitoring of intestinal serotonin levels in intact zebrafish embryos.