Double-Blind Placebo-Controlled Study of Milnacipran in Hospitalized Patients with Major Depressive Disorders

Mâcher, Jean-Paul; Sichel, J P; Serre, C.; Frenckell, R. von; Huck, J. C.; Demarez, Jean-Paul

doi:10.1159/000118596

Cited by 47 publications

(22 citation statements)

References 5 publications

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“…Furthermore, minalcipran which, like nisoxetine, selectively blocks the reuptake of NE (Blier et al 1993), has been reported to be an effective antidepressant in humans (Macher et al 1989;von Frenckell et al 1990). It is thus possible that the desensitization of u2-adrenergic heterorecep tors on 5-HT terminals contributes to the therapeutic action of these drugs.…”

Section: Discussionmentioning

confidence: 99%

Electrophysiologic Evidence for Desensitization of α2-Adrenoceptors on Serotonin Terminals Following Long-Term Treatment with Drugs Increasing Norepinephrine Synaptic Concentration

Mongeau

Montigny

Blier

1994

Neuropsychopharmacol

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Previous results from our laboratory have indicated that small intravenous doses of the u2-adrenergic agonist clonidine increase serotonin (5-HT) neurotransmission by attenuating the release of endogenous norepinephrine (NE), as a result of the activation of u2-adrenergic autoreceptor on NE neurons, and that high doses of clonidine decrease 5-HT neurotransmission by directly activating u2-adrenergic heteroreceptors on 5-HT terminals. The aim of the present study was to assess whether antidepressant treatments that increase the synaptic concentration of NE or 5-HT alter the ability of clonidine to modulate 5-HT neurotransmission through these two u2-adrenoceptors. Rats were treated for 3 weeks with 0.75 mglkg per day of befloxatone (a reversible inhibitor of monoamine oxidase A), 10 mglkg per day of ni soxetine (a selective NE reuptake inhibitor), 10 mglkg per day of paroxetine (a selective 5-HT reuptake inhibitor)

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Section: Discussionmentioning

confidence: 99%

Electrophysiologic Evidence for Desensitization of α2-Adrenoceptors on Serotonin Terminals Following Long-Term Treatment with Drugs Increasing Norepinephrine Synaptic Concentration

Mongeau

Montigny

Blier

1994

Neuropsychopharmacol

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“…143 A strong dose-response effect on tolerability was reported, but both 50 mg and 100 mg doses were well tolerated. 144,177 Discontinuation rates due to adverse events were similar to those with placebo. The most common adverse event was transient mild to moderate nausea.…”

mentioning

confidence: 66%

“…176,215,218,220 Milnacipran 50 mg was significantly more effective than placebo in the treatment of MDD. 176,177 Comparison of milnacipran with other antidepressants, such as SSRIs and TCAs, demonstrated no significant differences in clinical response or remission rates in the acute phase. 178 …”

Section: Milnacipranmentioning

confidence: 99%

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Getting the balance right: Established and emerging therapies for major depressive disorders

Perović

Jovanović²,

Miljković³

et al. 2010

NDT

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Major depressive disorder (MDD) is a common and serious illness of our times, associated with monoamine deficiency in the brain. Moreover, increased levels of cortisol, possibly caused by stress, may be related to depression. In the treatment of MDD, the use of older antidepressants such as monoamine oxidase inhibitors and tricyclic antidepressants is decreasing rapidly, mainly due to their adverse effect profiles. In contrast, the use of serotonin reuptake inhibitors and newer antidepressants, which have dual modes of action such as inhibition of the serotonin and noradrenaline or dopamine reuptake, is increasing. Novel antidepressants have additive modes of action such as agomelatine, a potent agonist of melatonin receptors. Drugs in development for treatment of MDD include triple reuptake inhibitors, dual-acting serotonin reuptake inhibitors and histamine antagonists, and many more. Newer antidepressants have similar efficacy and in general good tolerability profiles. Nevertheless, compliance with treatment for MDD is poor and may contribute to treatment failure. Despite the broad spectrum of available antidepressants, there are still at least 30% of depressive patients who do not benefit from treatment. Therefore, new approaches in drug development are necessary and, according to current research developments, the future of antidepressant treatment may be promising.

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“…The biochemical and pharmacological pro®le of milnacipran suggested that the drug would be therapeutically eective and well tolerated. This has been borne out by the results of placebo-controlled and open label trials of the antidepressant ecacy of milnacipran, as well as of comparative trials with tricyclic antidepressants (TCAs) and selective serotonin reuptake inhibitors (SSRIs) (Kasper et al, 1996;Lecrubier et al, 1996;Lopez-Ibor et al, 1996;Macher et al, 1989;Serre et al, 1986).…”

Section: Introductionmentioning

confidence: 99%

Milnacipran: The Clinical Properties of a Selective Serotonin and Noradrenaline Reuptake Inhibitor (SNRI)

Lecrubier¹

1997

Hum. Psychopharmacol. Clin. Exp.

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Double-Blind Placebo-Controlled Study of Milnacipran in Hospitalized Patients with Major Depressive Disorders

Cited by 47 publications

References 5 publications

Electrophysiologic Evidence for Desensitization of α2-Adrenoceptors on Serotonin Terminals Following Long-Term Treatment with Drugs Increasing Norepinephrine Synaptic Concentration

Electrophysiologic Evidence for Desensitization of α2-Adrenoceptors on Serotonin Terminals Following Long-Term Treatment with Drugs Increasing Norepinephrine Synaptic Concentration

Getting the balance right: Established and emerging therapies for major depressive disorders

Milnacipran: The Clinical Properties of a Selective Serotonin and Noradrenaline Reuptake Inhibitor (SNRI)

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