Serotonin Function and Mechanism of Action of Antidepressant Treatment

Charney, Dennis S.; Heninger, George R.; Sternberg, David E.

doi:10.1001/archpsyc.1984.01790150049008

Cited by 141 publications

(31 citation statements)

References 61 publications

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“…Tricyclic antidepressants, e.g. clomipramine, amitriptyline, imipramine and desipramine, potentiate L-tryptophan-stimulated prolactin release (Charney et al, 1984;Anderson & Cowen, 1986) and, given alone in sufficiently large acute doses, also induce secretion of prolactin (Calil et al, 1984;Laakmann et al, 1985Laakmann et al, , 1986Nutt et al, 1987). Furthermore, fenfluramine, which releases 5-HT and inhibits its neuronal reuptake, stimulates prolactin secretion in man (Quattrone et al, 1983;Lewis & Sherman, 1985), as also does the putative 5-HT receptor agonist m-chlorophenylpiperazine (Mueller et al, 1986).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of monoamine oxidase by moclobemide: effects on monoamine metabolism and secretion of anterior pituitary hormones and cortisol in healthy volunteers.

Koulu

Scheinin

Kaarttinen

et al. 1989

Brit J Clinical Pharma

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1. Single oral doses (100, 200 and 300 mg) of moclobemide, a reversible inhibitor of monoamine oxidase (MAO) with predominant effects on the A‐ type of the enzyme, were administered to eight young, healthy male volunteers in a double‐blind, random‐order, placebo‐controlled study. The investigation was thereafter continued in an open fashion by administering a single 10 mg dose of the MAO‐B inhibitor deprenyl to the same subjects. 2. Deamination of catecholamines was powerfully and dose‐dependently inhibited by moclobemide, as evidenced by up to 40% decreases in the urinary excretion of deaminated catecholamine metabolites, corresponding increases in the excretion of non‐ deaminated, methylated metabolites, and up to 79% average decreases in the plasma concentration of 3,4‐dihydroxyphenylglycol (DHPG), a deaminated metabolite of noradrenaline (NA), and up to 75% average decreases in the plasma concentrations of 3,4‐dihydroxyphenylacetic acid (DOPAC), a deaminated metabolite of dopamine. The urinary excretion of 5‐hydroxyindoleacetic acid (5‐HIAA) was only slightly reduced. In contrast, deprenyl, in a dose which almost totally inhibited MAO‐B activity in blood platelets, did not appreciably affect the plasma concentrations of DHPG or DOPAC. 3. Due to the rapid, reversible, dose‐dependent and MAO‐A specific effect of moclobemide on plasma concentrations of DHPG, it is suggested that DHPG in plasma may be a useful indicator of the magnitude and duration of MAO‐A inhibition in man. 4. Sympatho‐adrenal function at rest was not significantly altered by moclobemide, as judged by unchanged plasma catecholamine concentrations and stable blood pressure and heart rate recordings. 5. Monoamine oxidase type B activity in blood platelets was slightly (less than 30%) and transiently inhibited after moclobemide. 6. The secretion of prolactin was dose‐dependently stimulated by moclobemide, whereas the plasma concentrations of growth hormone (hGH) and cortisol remained unchanged.

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Section: Discussionmentioning

confidence: 99%

Inhibition of monoamine oxidase by moclobemide: effects on monoamine metabolism and secretion of anterior pituitary hormones and cortisol in healthy volunteers.

Koulu

Scheinin

Kaarttinen

et al. 1989

Brit J Clinical Pharma

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“…Disturbed serotonin function in Major Depression has been evident from in vivo challenge studies of serotonin responsivity using clomipramine (Leatherman et al 1993), tryptophan (Charney et al 1984), ipsapirone (Lesch 1991), m-chlorphenylpiperazine (mCPP) (Quested et al 1997), 1-5 hydroxytryptophan (Maes and Meltzer 1995), and fenfluramine (Mann et al 1995Siever et al 1984;Shapira et al 1993Shapira et al , 1992aKasper et al 1990;Flory et al 1998;Malone et al 1996;Mokrani et al 1997).…”

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Prolactin Response to dl-Fenfluramine Challenge before and after Treatment with Paroxetine

Dulchin¹

2001

Neuropsychopharmacology

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“…Preclinical and clinical evidences suggest that an enhancement in 5-HT function may be a common denominator in the therapeutic action of most antidepressant treatments (Blier et al 1990;Charney et al 1984). If TSD exerts its effect through an increase in brain 5-HT activity, the coadministration of pindolol should result in an enhanced antidepressant effect, similar to that observed with pindolol and serotonergic drugs.…”

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confidence: 93%

“…Since somatodendritic 5-HT 1A autoreceptors are responsible of the self-inhibition of 5-HT on serotonergic neurons, it has been hypothesized that the combination of selective serotonin reuptake inhibitors (SSRIs) with pindolol could reduce the self-inhibition of serotonergic transmission, thus enhancing the antidepressant effect of the former compounds (Artigas 1995;Artigas et al 1996). Recent double-blind placebo-controlled studies confirmed, with one exception (Berman et al 1997), that pindolol hastens the antidepressant effect of SSRIs Tome et al 1997aTome et al , 1997bZanardi et al 1997;Zanardi et al 1998), while controversial results have been reported in studies on resistant depression (e.g., Artigas et al 1994;Blier and Bergeron 1995;Moreno et al 1997).Preclinical and clinical evidences suggest that an enhancement in 5-HT function may be a common denominator in the therapeutic action of most antidepressant treatments (Blier et al 1990;Charney et al 1984). If TSD exerts its effect through an increase in brain 5-HT activity, the coadministration of pindolol should result in an enhanced antidepressant effect, similar to that observed with pindolol and serotonergic drugs.…”

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confidence: 99%

Sustained Antidepressant Effect of Sleep Deprivation Combined with Pindolol in Bipolar Depression A Placebo-Controlled Trial

Smeraldi

Benedetti

Barbini

et al. 1999

Neuropsychopharmacology

102

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Total sleep deprivation (TSD) shows powerful but transient clinical effects in patients affected by bipolar depression. Pindolol blocks the serotonergic 5-HT KEY WORDS : Sleep deprivation; Pindolol; Bipolar disorder; LithiumTotal sleep deprivation (TSD) causes a marked but transient improvement of depressive symptomatology in bipolar depressed patients: it acts rapidly and with a response rate of about 60%, but the dramatic mood improvement is usually followed by an early relapse (i.e., within the first days after TSD) which lessens the clinical usefulness of this treatment (Wu and Bunney 1990). Several studies, indeed, showed better clinical responses with the combination of sleep deprivation and antidepressant drugs (Leibenluft and Wehr 1992). In particular, positive interactions were reported with lithium, fluoxetine, nortryptiline, clomipramine, desipramine, and amitriptyline (e.g., Elsenga and Van den Hoofdakker 1982/1983Baxter et al. 1986;Shelton and Loosen 1993;Szuba et al. 1994;Kuhs et al. 1996;Benedetti et al. 1997), while negative interactions were observed with trimipramine and amineptine (HolsboerTrachsler et al. 1994;Benedetti et al. 1996).Though several hypotheses have been proposed, the mechanism of action of TSD is still unclear. From a neurochemical point of view, sleep deprivation enhances the functioning of several neurotransmitter systems including brain serotonin (5-HT) pathways, which physiologically show the highest activity during behavioral arousal and the lowest during sleep (Fornal and Jacobs 1988). In particular, preclinical research showed that From the Istituto Scientifico Ospedale San Raffaele, Department of Neuropsychiatric Sciences, University of Milan, School of Medicine, Milan, Italy.Address correspondence to: Prof. Enrico Smeraldi, Istituto Scientifico Ospedale San Raffaele, Department of Neuropsychiatric Sciences, Via Prinetti 29, 20127 Milano, Italy. Received October 20, 1997; revised March 4, 1998; accepted April 13, 1998. N EUROPSYCHOPHARMACOLOGY 1999 -VOL . 20 , NO . 4 Sustained Antidepressant Effect of Sleep Deprivation 381 changes in the activity of brain 5-HT pathways after sleep deprivation included an increase in the serotonergic neuronal activity in the dorsal raphe nucleus (DRN) of cats (Gardner et al. 1997), an increase in brain 5-HT turnover in rats and hamsters (Hery et al. 1970;Cramer et al. 1973;Asikainen et al. 1995), and an increase in behavioral responsiveness to 5-HT precursors (Santos and Carlini 1983). In agreement with these findings, a clinical study showed that in human depressed females sleep deprivation led to an enhanced prolactine response to tryptophan, an effect mediated by serotonergic pathways (Salomon et al. 1994).Preclinical studies showed that changes in 5-HT function due to TSD involve a reduction in sensitivity of 5-HT 1A autoreceptors. In rats, Maudhuit et al. (1996) showed that REM sleep deprivation reduced the inhibitory response of serotonergic DRN neurons to citalopram, an effect mediated by 5-HT 1A autoreceptors stimulatio...

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Serotonin Function and Mechanism of Action of Antidepressant Treatment

Cited by 141 publications

References 61 publications

Inhibition of monoamine oxidase by moclobemide: effects on monoamine metabolism and secretion of anterior pituitary hormones and cortisol in healthy volunteers.

Inhibition of monoamine oxidase by moclobemide: effects on monoamine metabolism and secretion of anterior pituitary hormones and cortisol in healthy volunteers.

Prolactin Response to dl-Fenfluramine Challenge before and after Treatment with Paroxetine

Sustained Antidepressant Effect of Sleep Deprivation Combined with Pindolol in Bipolar Depression A Placebo-Controlled Trial

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