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1. Fluvoxamine is a potent serotonin re-uptake inhibitor, with little or no noradrenergic or anticholinergic activity. 2. The results of three studies using an almost identical protocol with a prospectively randomized, double-blind design comparing fluvoxamine and chlorimipramine are presented. 3. In a population of 98 subjects suffering from a variety of depressive conditions, there was a marked improvement over four weeks in both groups. dosage was maintained between 150 and 300 mg per day. 4. There were no changes of clinical importance in vital signs, hematology or biochemistry, but pulse rates increased in the chlorimipramine group. 5. There were fewer concurrent signs and symptoms in the fluvoxamine group, especially those attributable to anticholinergic activity.
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Untreated cLH rats showed significantly lower glucose and higher taurine concentrations compared to WT animals. Besides alterations on these metabolites, ECS increased glutamate in WT and cLH and choline in cLH rats. Moreover, correlations between glutamate and GABA concentrations with learned helpless behaviour were revealed.
Although pindolol can accelerate the antidepressant action of selective serotonin reuptake inhibitors in previously untreated patients, it does not elicit a rapid clinical response in treatment-resistant patients within a 10-day period.
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The basis of the treatment of painful diabetic neuropathy is the use of drugs that block the transmission of pain (antineuritics) and a good metabolic control of underlying disease.
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Drug's effect was studied on rat corpus cavernosum (CC) and SV in vitro, and on the changes in intracavernosal pressure (ICP) after IC injection and intraluminal pressure (ILP) of the SV after hypogastric nerve stimulation (HNS), respectively.
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The final results of treatment with 4 antidepressants (amitriptyline, imipramine, chlorimipramine and mianserine) in 80 patients with endogenous depression were analyzed with respect to their pre-treatment levels of urinary MHPG. The analysis revealed that MHPG measurements were of no practical value in predicting individual response to antidepressants.
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The effects of chronic administration (28 days s.c. via osmotic minipumps) of the antidepressants phenelzine sulphate, desipramine hydrochloride and clomipramine hydrochloride (each at 10 mg/kg per day) on dopamine function have been measured in rats. Both phenelzine and desipramine attenuated the suppression of locomotor activity induced by apomorphine hydrochloride (0.05 mg/kg s.c. 15 min). Clomipramine did not affect the behavioural response to apomorphine. Analyses of brain tissue from these animals using the radioligand [3H]GBR 12935 revealed that there were no changes in dopamine uptake site density or affinity following the administration of phenelzine, desipramine or clomipramine. Analyses of brain monoamine oxidase activity and tricyclic levels were used to confirm the efficacy of the drug administration protocol. These data indicate that changes in dopamine uptake site density do not mediate antidepressant-induced changes in behavioural responses to apomorphine.
Clinicians should be aware that removing a serotonin-2a (S-HT2a) antagonist 1mm a treatment regimen including an agent that increases serotonin in the synaptic cleft may worsen clozapine withdrawal or potentially result in serious adverse drug reactions, such as serotonin syndrome.
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Intraperitoneal injection of a mixture of collagenase (300 U) and amitriptyline (Laroxyl*, 3 mg) induce no lesions in contrast with the severe effects of collagenase alone. Also, a complete resistance to intraperitoneal collagenase injection is observed when preceded by 3 intramuscular injections of the same mixture (associated with Freund's incomplete adjuvant). This is due to the development of collagenase antibodies, as demonstrated by nephelometry and immunodiffusion. These facts show that amitriptyline neutralizes the enzymatic properties of collagenase, without alterring its antigenicity. We propose to call this new substance anacollagenase. Such a phenomenon has never been observed with a drug. However we got identical results with other tricyclic depressants (clomipramine, imipramine, doxepine, iprindole). The mechanism of the transformation of collagenase into anacollagenase is not yet explained.
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This small, nonrandomized medicated sample analyzed under non-double-blind conditions shows no difference in the efficacy of clomipramine and sulpiride under post hoc analysis. Rather, the side effects that occurred in patients on clomipramine indicate a more frequent use of SSRI to increase compliance as regards medication intake.
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A developmental study has been made of spontaneous neuronal activity within the pontine reticular formation (giant cell field: FTG) of the rat between one week and one month after birth. Through day 14, the recorded FTG neurons discharged more frequently during quite sleep (QS) than was generally true in older animals. In addition, they were active to the same extent during active-sleep (AS) as during waking-with-movements (AW). In contrast, most of the cells recorded from day 15 on were considerably more active during AS and AW, relative to the QS level, than had hitherto been the case. This new class of neurons, in turn, fell into two sub-groups, one of which was most active during AW while the other was more active during AS. Clomipramine selectively suppressed AS along with the neuronal activity patterns associated with it, and in many cases the QS firing level was even lower than it had been prior to the injection. It is concluded that FTG unit activity is an excellent monitor for controlling the effectiveness of experimental manipulations of AS but is probably not involved in its generation.
We have developed and validated a high content screening approach that can be used in any ordinarily equipped cell biology laboratory employing exclusively freely available open-source software in order to find novel modulators of adhesion and cell spreading. The versatility and adjustability of the whole screening method will enable not only centers specialized in high-throughput screens but most importantly also labs not routinely employing screens in their daily work routine to investigate the effects of a wide range of different compounds or siRNAs on adhesion and adhesion-modulating molecules.
An isocratic, high-performance liquid chromatography method has been developed for simultaneous determination of the tricyclic antidepressant clomipramine and six metabolites: desmethylclomipramine, 2- and 8-hydroxy-clomipramine, 2- and 8-hydroxydesmethylclomipramine and didesmethyl-clomipramine in plasma and urine. In addition, clomipramine N-oxide was determined in the unconjugated fraction of urine. The method is based on a three-step liquid-liquid extraction, the chromatographic eluent was 30% acetonitrile and 70% aqueous sodium perchlorate solution, pH 2.5, and the UV detection was performed at 220 nm. The method was applied to the analysis of samples followed by oral doses of clomipramine to patients and healthy volunteers.
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Infusion of lipid emulsion resulted in greater survival in this rabbit model of intravenous clomipramine toxicity. Plasma exchange performed in conjunction with administration of lipid emulsion failed to result in significant extracorporeal clomipramine elimination. Intravascular lipid sequestration of clomipramine appears an inadequate sole explanation for the beneficial effects of lipid emulsion.
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Administration of fluvoxamine or sertraline to patients for an adequate duration is recommended as the first-line prescription for OCD, and augmentation therapy with risperidone, olanzapine, or quetiapine is recommended for refractory OCD.
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We report the clinical and therapeutic features of three patients with an obsessive-compulsive syndrome that emerged during the course of panic disorder. The DSM-IV criteria for panic disorder places central attention on the patient's phobic responses to the panic attacks and their perceived consequences. These phobic responses may develop into a syndrome that closely resembles obsessive-compulsive disorder (OCD) but typically responds to conventional anti-panic approaches. Our cases suggest that patients with OCD should be probed for an underlying panic disorder. This 'panic disorder-related subtype of OCD' may be associated with an excellent treatment response and increased rates of remission.
[3H]6-Nitroquipazine is a new, suitable radioligand for studying the uptake system for 5-hydroxytryptamine (5-HT; serotonin). In the present study, inhibition by drugs of the binding of [3H]6-nitroquipazine to uptake sites for 5-HT in the cerebral cortex of the rat was investigated. The inhibition of 5-HT and several inhibitors of the uptake of 5-HT (paroxetine, clomipramine, citalopram, Z-norzimelidine, fluoxetine, imipramine, desipramine and 5-methoxytryptoline) against the binding of [3H]6-nitroquipazine to membranes from the cortex of the rat were the same and competition curves indicated a single population of binding sites. The addition of 5-HT and the tricyclic inhibitors of the uptake of 5-HT, imipramine, clomipramine and desipramine, all produced changes in the apparent dissociation constant (Kd), without changes in the number of binding sites (Bmax). Also, the non-tricyclic inhibitors of the uptake of 5-HT, paroxetine, citalopram, fluoxetine and Z-norzimelidine, and 5-methoxytryptoline, all produced changes in Kd values without changes in the Bmax. These results suggest that all the drugs used in this experiment exhibited competitive interactions with the binding of [3H]6-nitroquipazine to uptake sites for 5-HT in the brain of the rat. These drugs may bind to common binding sites, which are likely to represent the substrate recognition sites for the uptake of 5-HT.
Despite the importance of 5-hydroxytryptamine (5-HT)(2C) (serotonin) receptors in the control of depressive states, actions of antidepressants at these receptors remain poorly characterized. This issue was addressed both in human embryonic kidney (HEK)-293 cells coexpressing unedited human 5-HT(2CINI) receptors and Galpha(q) protein and in cultured mouse cortical neurons. Indicative of constitutive activity, the inverse agonist SB206,553 decreased basal inositol phosphate (IP) production in HEK-293 cells. The tetracyclic antidepressants mirtazapine and mianserin likewise suppressed basal IP formation. Conversely, the tricyclics amitriptyline and clomipramine, the m-chlorophenylpiperazine derivatives trazodone and nefazodone, and the 5-HT reuptake inhibitors fluoxetine and citalopram were inactive alone, although they blocked 5-HT-induced IP production. Inverse agonist actions of 5-methyl-1-(3-pyridylcarbamoyl)-1,2,3,5-tetrahydropyrrolo[2,3-f]indole (SB206,553) and mirtazapine were abolished by the neutral antagonist 6-chloro-5-methyl-1-[6-(2-methylpyridin-3-yloxy)pyridin-3-ylcarbamoyl]indoline (SB242,084), which was inactive alone. As assessed by confocal microscopy and enzyme-linked immunosorbent assay, prolonged treatment of HEK-293 cells with SB206,553, mirtazapine, or mianserin, but not the other antidepressants, enhanced cell surface expression of 5-HT(2C) receptors: 5-HT-induced IP production was also increased, and both these actions were blocked by SB242,084. Cortical neurons were shown by reverse transcription-polymerase chain reaction to predominantly express constitutively active 5-HT(2C) receptor isoforms. Prolonged pretreatment with SB206,553 or mirtazapine triggered an otherwise absent 5-HT-induced elevation in cytosolic Ca(2+) concentrations. SB242,084, which was inactive alone, abolished these effects of SB206,553 and mirtazapine. In conclusion, the tetracyclic antidepressants mirtazapine and mianserin, but not other clinically established antidepressants, suppress constitutive activity at recombinant and native 5-HT(2C) receptors. The clinical significance of inverse agonist versus neutral antagonist properties both during and after drug administration will be of interest to elucidate.
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An attempt was made to measure the effects of depressive illness and of clomipramine (Anafranil) therapy in doses of 30 mg and 75 mg daily on sexual appetite and performance. A special questionnaire was devised to gather information on sexual habits before illness, during illness and following treatment. It proved difficult to differentiate between the beneficial effects of recovery from depression and the possible adverse drug effects on sexual activity. Two patients dropped out of the study because of supposed sexual side-effects--a male with ejaculatory difficulties and a female with orgasmic impotence. Fifty-four patients completed the sexual questionnaire and a four-week course of clomipramine. There were nineteen males and thirty-five females. Sixty-eight per cent of males and 57% of females had their 'sex life' impaired by depressive illness. Coital rate was decreased and depression interfered with performance and satisfaction. Clomipramine therapy seemed to have advantageous and disadvantageous effects. The advantageous effects were probably associated with improvement in depressive illness. There was evidence that clomipramine had an adverse effect sexually in 26% of males and 14% of females. The effect was dose-related in females.
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Depressed patients who had responded to either cognitive therapy, pharmacotherapy or the 2 treatments combined, were followed up retrospectively over a period of 2 years. There were significantly more relapses at 6 months in the pharmacotherapy group compared to the combined treatment group and the 2 cognitive therapy groups together. The number of individuals who relapsed at some point over the 2 years was significantly higher in the pharmacotherapy group than in either of the cognitive therapy groups. When hospital patients were considered separately, significantly more patients in the pharmacotherapy group relapsed over the 2 years compared to the 2 cognitive therapy groups combined. Methodological problems of naturalistic follow-up studies are discussed and the prophylactic potential of cognitive therapy is discussed relative to continuation drug treatment.