Disease relevance of Nialamide

• It neither antagonized the effects of reserpine in rats (hypothermia, ptosis) nor potentiated the effects of amphetamine (in mice and rats), nialamide or L-dopa (in mice) on locomotor activity [1].
• Delay in nerve degeneration after sympathectomy of the submaxillary gland of the rat by treatment with pargyline, nialamide or beta-TM-10 [2].
• Rats were given subcutaneously 50 mg/kg body weight of nialamide in depot form every other day after 25 weeks of oral treatment with MNNG [3].
• Mutagenic effect of nialamide on Salmonella typhimurium [4].
• Prolonged alternate-day administration of nialamide caused a significant increase in the incidence and number of gastric cancers of the glandular stomach in week 52 [3].

Psychiatry related information on Nialamide

• Nialamide (100 mg/kg, i.p.) and pargyline-HCl (100 and 200 mg/kg, i.p.) caused marked reduction of the conditioned suppression but did not increase the motor activity of the non-shocked mice, and tranylcypromine-HCl (10 and 20 mg/kg, i.p.) did not cause reduction of the conditioned suppression [5].
• Ganglioside pretreatment enhanced the anti-immobility effect induced in the forced swim test after a chronic treatment with desipramine, mianserin, clomipramine, nialamide or repeated electroconvulsive shock in mice [6].
• Nialamide did not depress the apomorphine-induced stereotyped behavior [7].
• Previous inhibition of monoamine oxidase activity obtained with nialamide increased evidently the inhibitory effect of the studied neuroleptics on the appearance of defensive conditioned reflex [8].
• Through a controlled double-blind study in 30 hospitalized patients affected with endogenous depression, the antidepressant action of the combination of nialamide+l-5-HTP has been evaluated and compared with a control group which only received nialamide (+ placebo) [9].

High impact information on Nialamide

• We now report that pargyline, nialamide and tranylcypromine, which inhibit both MAO-A and MAO-B, when administered to mice before MPTP, protect against MPTP-induced dopaminergic neurotoxicity [10].
• Rats that were pretreated with the nonspecific MAO inhibitor nialamide (200 mg/kg) showed a greater rise in meal-induced serum gastrin than did untreated controls [11].
• Some had dopamine beta-hydroxylase-like (DBH-IR) immunoreactivity, but none contained detectable catecholamines, even after treatment with nialamide and L-DOPA [12].
• There was no detectable elevation in the plasma insulin concentration accompanying the hypoglycaemic response to smaller doses of 5HTP in nialamide treated mice [13].
• Subsensitivity of the beta-adrenergic receptor-linked adenylate cyclase system of rat pineal gland following repeated treatment with desmethylimipramine and nialamide [14].

Chemical compound and disease context of Nialamide

• These results suggest that the reduced locomotor activity response of old rats to the intra-accumbens injections of dopamine after nialamide pretreatment may be due to the reduced ability of nialamide to inhibit monoamine oxidase (and dopamine metabolism) in these animals [15].
• Octopamine (100, 250 and 500 micrograms/rat i.v.c.) exerted a stimulating effect on the central nervous system in rats, which was evidenced by increased spontaneous and basal motor activity, increased exploratory activity in the free-field test, and also increased motor activity in reserpinised rats pretreated with alpha-MT or nialamide [16].

Biological context of Nialamide

• The decrease in body temperature elicited by a low dose of 5-methoxy-N, N-dimethyltryptamine (5MeODMT, 1 mg/kg) also was diminished in rats treated chronically with nialamide [17].
• Injection of a monoamine oxidase (MAO) inhibitor (nialamide) into the uterus of an anaesthetized and laparotomized rat on day 20 of pregnancy severely disturbed parturition [18].
• L-5-Hydroxy-tryptophan (L-5HTP) induced penile erections when co-administered with nialamide and the peripheral decarboxylase inhibitor benserazide, indicating that the site of action for inducing penile erections is within the central nervous system [19].
• The effects of nialamide, a monoamine oxidase inhibitor, on the incidence, number, and histology of gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were investigated in male Wistar rats [3].
• A study was made in fast growing rats (65 g) of the nutritive effects of protein and the effect on different organs when influenced by nialamide (IMAO), administered at a dosage of 10 mg/100 g diet, with food intake controlled (pair fed) [20].

Anatomical context of Nialamide

• In high spinal paralysed cats electromyograms were recorded from nerves supplying lumbar back muscles (longissimus dorsi) and abdominal muscles (obliquus abdominis externus) during fictive locomotion induced by I.V. injection of nialamide and L-DOPA [21].
• The CAR-trained rats, conditioned to avoid an electric shock, were administered AMPT (150 mg/kg at -24 h and 50 mg/kg at -1 h, both IP), nialamide (80 mg/kg IP at -1 h) and saline (1 microliter) or DA (5 or 10 micrograms/microliters, dissolved in 1 microliter saline, at time 0) directly into the nucleus accumbens [22].
• In support of this hypothesis, nialamide (25-100 mg/kg i.p.), which inhibited monoamine oxidase activity in limbic forebrain homogenates of old, mature and young rats, was a less effective inhibitor of this enzyme in the old rats [15].
• To test whether these changes in effectiveness were localized to sites within the spinal cord, the cord was transected in some decerebrate animals and stepping induced by the administration of L-DOPA L-3-4 dihydroxyphenylalanine (L-DOPA) and Nialamide [23].
• Nonhormonal drugs--diphenylhydantoin and nialamide, which act on the central nervous system and have no known endocrine activity--were given to two groups of women with distinct types of electroencephalographic patterns in an effort to regulate menstrual disorders [24].

Associations of Nialamide with other chemical compounds

• The region-specific effects of 5-HT and nialamide in glial co-cultures suggest that raphe and mesencephalic glia may express different capacities for 5-HT uptake, receptors, and/or monoamine oxidase (MAO) activities [25].
• The AMPH was dissolved in saline (1 microliter; pH, 5.5-6.0), while DA was dissolved in N2 bubbled distilled H2O (1 microliter; pH, 5.5-6.0) and the animals were pretreated with nialamide (50 mg/kg) intraperitoneally 1 hr before DA or DA-vehicle injection [26].
• 3 Fluorescence brightness due to accumulation of noradrenaline was increased if animals were pretreated with the monoamine oxidase inhibitor drug, nialamide [27].
• A wide variety of phenylethylamine derivatives were injected bilaterally into the nucleus accumbens of rat following a nialamide pretreatment and hyperactivity was recorded [28].
• Consistent with this observation, the concentrations of the dopamine metabolites, homovanillic acid and dihydroxyphenylacetic acid were higher in nialamide-pretreated old rats than in young and mature rats, suggesting that there was a smaller inhibition of the metabolism of dopamine in the limbic forebrain of old rats after nialamide pretreatment [15].

Gene context of Nialamide

• 3. The effects of reserpine and/or nialamide on hepatic COMT and MAO were studied in control and 20-day-pregnant rats [29].
• The treatment of rats for 4 or 7 days with nialamide (40 mg/kg, twice daily) resulted in a suppression of the hypothermic effect of the 5-HT1A agonist 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT, 0.05-0.25 mg/kg, SC) [17].
• Pretreatment with the 5-HT2 antagonist ritanserin 1 and 10 mg/kg SC reduced the hypermotility produced by nialamide 200 mg/kg SC, but the 5-HT1 antagonist L-propranolol 10 mg/kg administered similarly was found inactive [30].
• When the parakeets were injected with 3H-5-HTP alone or pretreated with drugs interfering with monoamine metabolism (e.g. R04-4602, nialamide) prior to injection of the label, the SRP cells always exhibited specific radioautographic reactions, in the regions of the dense secretory granules of the cell body and asynaptic pedicles [31].
• At an early stage after transplantation (3 days), TH-positive neurons appeared in grafts that had and had not been pretreated with a monoamine oxidase inhibitor (MAOI, Nialamide), while serotonin-positive neurons were demonstrated only in the grafts that had undergone MAOI pretreatment [32].

Analytical, diagnostic and therapeutic context of Nialamide

• After premedication with nialamide and DOPA, naloxone facilitated or, if a rhythm was absent, induced the slow-frequency DOPA type of rhythm [33].
• (2) "Fictive locomotion", the centrally generated rhythmic synaptic drive produced in paralyzed, decerebrate animals by stimulation of the mesencephalic locomotor region or intravenous injection of L-DOPA and Nialamide, was monitored by recording electroneurograms from the central end of cut motor nerves [34].
• A steady locomotor rhythm was induced by injection of nialamide and L-dopa and the influence of electrical stimulation (trains of 50-1000 ms) of FRA (joint, cutaneous, and group II and III muscle afferents) onto this rhythm was tested [35].
• Using this relatively low dose of nialamide, almost no reflex response was seen in the control group [36].
• A method for provoking EEG abnormalities by administration of nialamide [37].

References