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PubMed1985

Monoamine oxidase inhibitors in the treatment of atypical depression.

In a 6-week, double-blind study outpatients diagnosed as suffering from atypical depression were treated with either isocarboxazid or placebo. Selection criteria were purposely broad so as to capture the entire range of patients so diagnosed. Patients were then subclassified along several symptomatic, syndromal, phenomenological, and diagnostic categories in order to identify clinical characteristics specifically responsive to isocarboxazid. Although isocarboxazid was clearly superior to placebo for the overall group of atypical depressives, the authors were by and large unable to identify subgroups specifically responsive to the monoamine oxidase inhibitor. A few factors correlated with better response to both isocarboxazid and placebo: no family history of alcoholism or sociopathy, lack of self-pity, and not meeting Research Diagnostic Criteria for major depressive disorder. The single item that was associated with a statistically significant advantage of isocarboxazid over placebo was loss of anticipatory pleasure. Clinical implications and suggestions for further research are discussed.

Adjustment Disorders↗
PubMed1995

MAOIs in the contemporary treatment of depression.

We review the literature on the effectiveness of the monoamine oxidase inhibitors (MAOIs) and present metaanalyses of controlled trials comparing the FDA-approved MAOIs with both placebo and comparator tricyclic antidepressants. For outpatients, metaanalyses with intent-to-treat samples revealed generally comparable overall efficacy for phenelzine, isocarboxazid, and tranylcypromine. Drug-placebo differences were 29.5% (+/- 11.1%) (phenelzine; nine studies), 41.3% (+/- 18.0%) (isocarboxazid; three studies), and 22.1% (+/- 25.4%) (tranylcypromine; three studies). For inpatients, phenelzine was 22.3% (+/- 30.7%) (five studies) more effective than placebo, whereas the isocarboxazid-placebo difference was lower (15.3%) (+/- 12.6%). Both phenelzine and isocarboxazid were significantly less effective than comparator tricyclics for inpatients, whereas tranylcypromine has not been adequately studied. Both phenelzine and tranylcypromine appear to be more effective than tricyclics in depressed outpatients with atypical features. Monoamine oxidase inhibitors are also effective treatments for outpatients who have failed to respond to tricyclic antidepressants. Our review also suggests (1) the FDA-approved MAOIs treat a somewhat different group of patients than tricyclics; (2) more severely depressed inpatients may not respond as well to MAOIs as to tricyclics; and (3) because of preferential MAOI responsivity, atypical or anergic depressions may be biologically different than classical depressions.

Antidepressive Agents, Tricyclic↗
PubMed1975

[Central action of beta-phenylethylamine derivatives. (4) Effects on spontaneous motor activity and body temperature of beta phenylethyamine derivatives injected into the brain in reserpine pretreated mice].

Effects on spontaneous motor activity and body temperature of beta-phenylethlamine derivatives injected into the cerebral ventricles in reserpine or reserpine and isocarboxazide pretreated mice were investigated with the following results. 1) Each injection of tyramine (40 mug) and dopamine (40 mug) increased the spontaneous motor activity measured by the photo-cell counters method in reserpinized mice. 2) Each injection of tyramine (40 mug), dopamine (40 mug) and beta-phenylethylamine (40 mug) increased the spontaneous motor activity measured by both the wheel cage and photo-cell counters methods in reserpine and isocarboxazide-pretreated mice, but noradrenaline (20 mug) and isoproterenol (80 mug) did not increase the spontaneous motor activity as determined by both methods. 3) The injection of tyramine (40 and 80 mug), dopamine (10 and 40 mug) and p-octopamine (40 mug) increased the body temperature in reserpine and isocarboxazide pretreated mice. 4) Tyramine, dopamine and p-octopamine caused a marked increase in the body temperature as compared with control injection in reserpine and isocarboxazide-pretreated mice, whereas isoproterenol had no influence on body temperature. Our results suggest that beta-phenylethylamine derivatives have different effects in reserpinized and non-pretreated states.

Animals↗
PubMed1991

Spectrophotometric determination of some MAO inhibitors using 7,7,8,8-tetracyanoquinodimethane and iodine monochloride.

Two simple and sensitive spectrophotometric methods are described for the assay of three MAO inhibitors: isocarboxazid, tranylcypromine sulphate and iproniazid phosphate. The first method is based on the formation of a highly coloured stable radical anion between the drug as an n-donor and 7,7,8,8-tetracyanoquinodimethane (TCNQ) as a pi-electron acceptor. Beer's law is obeyed in the concentration range 0.2-3, 0.2-4 and 0.5-4 micrograms ml-1 for isocarboxazid, tranylcypromine sulphate and iproniazid phosphate, respectively. The second method involves the use of iodine monochloride (ICl) as an sigma-acceptor. It was found that ICl reacts quantitatively only with isocarboxazid and tranylcypromine sulphate; with iproniazid phosphate results were very poor. Beer's law is obeyed in the concentration range 2-20 micrograms ml-1 for both drugs. The optimum experimental parameters for colour production in each case were determined. The percentage recoveries obtained were in accordance with those obtained by the official methods. The proposed methods are characterized by high sensitivity.

Chlorides↗
PubMed1961

Relative activity of some inhibitors of mono-amine oxidase in potentiating the action of tryptamine in vitro and in vivo.

Several known inhibitors of mono-amine oxidase (iproniazid, isocarboxazid, nialamide, phenelzine, pheniprazine and tranylcypromine) were tested for their ability to (i) inhibit the mono-amine oxidase activity of a rat brain mitochondrial preparation in vitro; (ii) potentiate the action of tryptamine on the isolated rat fundal strip preparation; and (iii) potentiate the acute toxicity of tryptamine in mice. There was some correlation between the order of potency of the drugs in the three tests, particularly in inhibiting the enzyme activity in the Warburg and in the tryptamine toxicity test in mice. Exceptions to this were isocarboxazid which had unexpectedly high activity on the rat fundal strip preparation, and tranylcypromine which was devoid of tryptamine-potentiation action on the rat fundus preparation although it inhibited rat brain mono-amine oxidase in vitro and potentiated the action of tryptamine in vivo. Tranylcypromine was considerably less active in inhibiting the mono-amine oxidase of rat fundus than rat brain tissue in vitro, while iproniazid and isocarboxazid had about the same potency on the enzyme from the two tissues.

Animals↗
PubMed1990

Efficacy of combined antidepressant therapy in resistant neurotic disorder.

A 35-year-old woman with persistent affective and phobic symptoms responded dramatically to a combination of isocarboxazid and amitriptyline, and this improvement was maintained over the next three-and-a-half years. Isocarboxazid was replaced by placebo, using double-blind procedure. The change to placebo was accompanied by a marked increase in anxiety and depressive symptoms, which resolved when active isocarboxazid was reintroduced. It is suggested that combined antidepressant therapy still has a place in the treatment of resistant neurotic disorder.

Adult↗
PubMed1993

Differential responses of rat hepatic microsomal carboxylesterase isozymes to glucocorticoids and pregnenolone 16 alpha-carbonitrile.

Differences in the responses to glucocorticoids and pregnenolone 16 alpha-carbonitrile (PCN) of three isozymes of hepatic microsomal carboxylesterase, namely RL1, RL2 and RH1, in male rats were studied. The administration of dexamethasone dose-dependently increased isocarboxazid hydrolase activity, whereas p-nitrophenyl acetate-hydrolyzing activity was decreased dose-dependently. Betamethasone, methylprednisolone and PCN also markedly increased isocarboxazid hydrolase activity. A radial immunodiffusion assay indicated that carboxylesterase reactive with antibodies was induced by these steroids. Carboxylesterase isozyme RL2 was strongly induced by dexamethasone, methylprednisolone and PCN. In contrast, RL1 and RH1 were decreased by dexamethasone, but not by the other steroids. Estradiol benzoate had a synergic effect on the PCN-induced increase of isocarboxazid hydrolase, but the actions of the glucocorticoids were not affected. It is concluded that hepatic microsomal carboxylesterase isozymes in rats differ considerably from each other in their response to various steroids. These data are also indicative of the importance of glucocorticoids in hepatic xenobiotic metabolism.

Animals↗
PubMed1980

[Effects of mianserin on functions of ascending and descending monoaminergic systems, using experimental models (author's transl)].

Studies were carried out to evaluate the antidepressant action of Mianserin as related to noradrenergic and serotonergic systems. The actions of known tricyclic anti-depressants were comparatively investigated together with Mianserin (Organon). Self-stimulation behavior induced by stimulation of the posterior hypothalamus and substantia nigra was unaffected by Mianserin and imipramine, was suppressed with chlorpromazine and markedly enhanced by methamphetamine. The enhancement due to methamphetamine was suppressed by both Mianserin and chlorpromazine, and was potentiated by imipramine. Mianserin, imipramine and amitriptyline enhanced the rolling movements induced by methamphetamine in rats in which the nigro-striatal dopaminergic system was destroyed by the injection of 6-hydroxydopamine. The excitation induced by ldopa administration, of isocarboxazid treated mouse was enhanced by Mianserin in doses over 25 mg/kg and by imipramine or amitriptyline. The excitation of MK-486 treated mouse, induced by L-5HTP was suppressed by Mianserin, nortriptyline augmented the excitation. The head twitches induced by 5HTP were reduced to 1/10 in onset frequency by Mianserin, 1 mg/kg, p.o. The suppressive potency of amitriptyline in this model was less than 1/5 of that of Mianserin. The potentiation of the flexor reflex of hind limbs of the spinal rat induced by the pretreatment with isocarboxazid and l-dopa, 20 hours after the reserpinization, was markedly suppressed by Mianserin and amitriptyline, but unaffected by imipramine nor chlorimipramine. The potentiation of the extensor reflex of hind limbs of the spinal rat, induced 20 hours after the reserpinization by pretreatment with isocarboxazid and 5-HTP was suppressed by Mianserin, even in a low dose of 0.5 mg/kg, and by amitriptyline in a dose of 10 mg/kg. As far as monoaminergic mechanisms are concerned, the mode of antidepresant action of Mianserin is probably different from that of tricyclic antidepressants.

5-Hydroxytryptophan↗
PubMed1972

Brain amine concentrations after monoamine oxidase inhibitor administration.

The concentrations of 5-hydroxytryptamine (5HT), noradrenaline, and dopamine were estimated post mortem in brain stem, hypothalamus, and caudate nucleus in 33 patients who had been treated with isocarboxazid, clorgyline, or tranylcypromine and 11 controls. Similar and highly significant increases in 5HT and noradrenaline concentration occurred with all three drugs. The distribution was unimodal, but about a quarter of the patients showed only a small increase in brain amines. Tranylcypromine seemed to have a significantly greater effect on dopamine in caudate nucleus and hypothalamus compared with isocarboxazid and clorgyline. In the doses used chlorpromazine did not reduce the amine concentrations. Four patients with Parkinson's syndrome had low concentrations of dopamine in caudate nucleus in spite of monoamine oxidase inhibitor administration.

Aged↗
PubMed1979

Controlled trial of trimipramine, monoamine oxidase inhibitors, and combined treatment in depressed outpatients.

A study was carried out in which 135 mildly or moderately depressed outpatients were randomly allocated to one of five groups receiving six weeks' treatment weith antidepressant drugs. The groups received a tricyclic antidepressant (trimipramine; mean dose 106 mg at night) or a monoamine oxidase inhibitor (MAOI) (phenelzine or isocarboxazid; mean doses 45 and 32 mg/day respectively), or a combination of the two (phenelzine plus trimipramine or isocarboxazid plus trimipramine). Various scales were used to measure depression before and at one, three, and six weeks of treatment, and results were assessed blindly. The tricyclic antidepressant was found to be consistently superior to the MAOIs and the combined treatments. Some differential indicators of response to the various antidepressants were found--for example, patients with initial complaints of dizziness, suicidal ideas, irritability, and insomnia and a longer duration of illness were more likely to respond to trimipramine--but these were of only modest significance. Side effects were not troublesome in any group. It is concluded that neither MAOIs nor MAOIs combined with tricyclic antidepressants are the treatment of first choice in unselected outpatients with mild or moderate depression.

Adult↗