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Chemical Compound Review

Nialamide     N-benzyl-3-(2-pyridin-4...

Synonyms: Nialamid, Niamidal, Isalizina, Nialamida, Niaquitil, ...
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Disease relevance of Nialamide


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


Biological context of Nialamide


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].


  1. The central action of pizotifen. Przegaliński, E., Baran, L., Palider, W., Siwanowicz, J. Psychopharmacology (Berl.) (1979) [Pubmed]
  2. Delay in nerve degeneration after sympathectomy of the submaxillary gland of the rat by treatment with pargyline, nialamide or beta-TM-10. Arbilla, S., Perec, C.J., Stefano, F.J. J. Pharmacol. Exp. Ther. (1977) [Pubmed]
  3. Promotion by nialamide of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats. Tatsuta, M., Iishi, H., Baba, M., Taniguchi, H. Jpn. J. Cancer Res. (1989) [Pubmed]
  4. Mutagenic effect of nialamide on Salmonella typhimurium. Stoltz, D.R., Bendall, R.D., Miller, C.T. Mutat. Res. (1976) [Pubmed]
  5. Effects of antidepressant drugs on a quickly-learned conditioned-suppression response in mice. Kameyama, T., Nagasaka, M., Yamada, K. Neuropharmacology (1985) [Pubmed]
  6. Gangliosides enhance the anti-immobility response elicited by several antidepressant treatments in mice. Córdoba, N.E., Basso, A.M., Molina, V.A., Orsingher, O.A. Psychopharmacology (Berl.) (1990) [Pubmed]
  7. Effects of penfluridol and other drugs on apomorphine-induced stereotyped behavior in monkeys. Shintomi, K., Yamamura, M. Eur. J. Pharmacol. (1975) [Pubmed]
  8. The effects of neuroleptics and nialamide on defensive conditoned reflex in rats. Plech, S., Drybański, A., Herman, Z. Acta physiologica Polonica. (1975) [Pubmed]
  9. 5-Hydroxytryptophan (5-HTP) and a MAOI (nialamide) in the treatment of depressions. A double-blind controlled study. Aliño, J.J., Gutierrez, J.L., Iglesias, M.L. International pharmacopsychiatry. (1976) [Pubmed]
  10. Protection against the dopaminergic neurotoxicity of 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine by monoamine oxidase inhibitors. Heikkila, R.E., Manzino, L., Cabbat, F.S., Duvoisin, R.C. Nature (1984) [Pubmed]
  11. Monoamine oxidase: an important intracellular regulator of gastrin release in the rat. Dial, E.J., Huang, J., Delansorne, R., Lichtenberger, L.M. Gastroenterology (1986) [Pubmed]
  12. Catecholaminergic properties of cholinergic neurons and synapses in adult rat ciliary ganglion. Landis, S.C., Jackson, P.C., Fredieu, J.R., Thibault, J. J. Neurosci. (1987) [Pubmed]
  13. Further studies on the effects of 5-hydroxytryptophan on plasma glucose and insulin in the mouse. Furman, B.L., Wilson, G.A. Diabetologia (1980) [Pubmed]
  14. Subsensitivity of the beta-adrenergic receptor-linked adenylate cyclase system of rat pineal gland following repeated treatment with desmethylimipramine and nialamide. Moyer, J.A., Greenberg, L.H., Frazer, A., Weiss, B. Mol. Pharmacol. (1981) [Pubmed]
  15. Effect of nialamide on the metabolism of dopamine injected into the nucleus accumbens of old rats. Cousin, K.M., Gerald, M.C., Uretsky, N.J. J. Pharmacol. Exp. Ther. (1986) [Pubmed]
  16. Central effects of octopamine administered into the lateral ventricle of rats. Kleinrok, Z., Jagiełło-Wójtowicz, E., Szkilnik, E. Acta physiologica Polonica. (1979) [Pubmed]
  17. Suppression of the hypo- and hyperthermic responses to 5-HT agonists following the repeated administration of monoamine oxidase inhibitors. Gudelsky, G.A., Koenig, J.I., Jackman, H., Meltzer, H.Y. Psychopharmacology (Berl.) (1986) [Pubmed]
  18. Effects of injections of monoamine oxidase inhibitor or saline into the uterus in late pregnancy on uterine catecholamine levels related to abnormal parturition in rats. Maltier, J.P., Cavaille, F. J. Endocrinol. (1975) [Pubmed]
  19. Drug-induced penile erections in rats: indications of serotonin1B receptor mediation. Berendsen, H.H., Broekkamp, C.L. Eur. J. Pharmacol. (1987) [Pubmed]
  20. Study of absorption and retention of nitrogen in fast growing rats--II. Influence of IMAO (nialamide). Barrionuevo, M., Reche, A., Campos, M.S., Mataix, F.J. Comp. Biochem. Physiol. C, Comp. Pharmacol. Toxicol. (1985) [Pubmed]
  21. Phasic modulation of trunk muscle efferents during fictive spinal locomotion in cats. Koehler, W.J., Schomburg, E.D., Steffens, H. J. Physiol. (Lond.) (1984) [Pubmed]
  22. alpha-methyl-p-tyrosine inhibition of a conditioned avoidance response: reversal by dopamine applied to the nucleus accumbens. Bracs, P.U., Jackson, D.M., Gregory, P. Psychopharmacology (Berl.) (1982) [Pubmed]
  23. Plasticity in reflex pathways controlling stepping in the cat. Whelan, P.J., Pearson, K.G. J. Neurophysiol. (1997) [Pubmed]
  24. Clinical investigation of the menstrual cycle. II. Neuroendocrine investigation and therapy of the inadequate luteal phase. Gautray, J.P., Jolivet, A., Goldenberg, F., Tajchner, G., Eberhard, A. Fertil. Steril. (1978) [Pubmed]
  25. Serotonin promotes region-specific glial influences on cultured serotonin and dopamine neurons. Liu, J., Lauder, J.M. Glia (1992) [Pubmed]
  26. Reduction of motor behavioral deficits in senescent animals via chronic prolactin administration. I. Rotational behavior. Joseph, J.A., Roth, G.S., Lippa, A.S. Neurobiol. Aging (1986) [Pubmed]
  27. The uptake kinetics and metabolism of extraneuronal noradrenaline in guinea-pig trachea as studied with quantitative fluorescence microphotometry. O'Donnell, S.R., Saar, N. Br. J. Pharmacol. (1978) [Pubmed]
  28. Characterisation of the mechanisms for hyperactivity induction from the nucleus accumbens by phenylethylamine derivatives. Costall, B., Naylor, R.J., Pinder, R.M. Psychopharmacology (Berl.) (1976) [Pubmed]
  29. Variation in activity of monoamine metabolizing enzymes in rat liver during pregnancy. Parvez, S., Parvez, S.H., Youdim, M.B. Br. J. Pharmacol. (1975) [Pubmed]
  30. Nialamide-induced hypermotility in mice treated with inhibitors of monoamine uptake, 5-HT antagonists and lithium. Buus Lassen, J. Psychopharmacology (Berl.) (1989) [Pubmed]
  31. The avian pineal organ. Distribution of exogenous indoleamines: a qualitative study of the rudimentary photoreceptor cells by electron microscopic radioautography. Collin, J.P., Calas, A., Juillard, M.T. Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale. (1976) [Pubmed]
  32. Immunohistochemical studies on the development of tyrosine hydroxylase- and serotonin-immunoreactive neurons in fetal dorsal raphe tissue transplanted into the anterior eye chamber of adult rats. Tanabe, T., Ueda, S., Sano, Y. Arch. Histol. Cytol. (1989) [Pubmed]
  33. Influence of opioids and naloxone on rhythmic motor activity in spinal cats. Schomburg, E.D., Steffens, H. Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale. (1995) [Pubmed]
  34. Peripheral and central control of flexor digitorum longus and flexor hallucis longus motoneurons: the synaptic basis of functional diversity. Fleshman, J.W., Lev-Tov, A., Burke, R.E. Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale. (1984) [Pubmed]
  35. Flexor reflex afferents reset the step cycle during fictive locomotion in the cat. Schomburg, E.D., Petersen, N., Barajon, I., Hultborn, H. Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale. (1998) [Pubmed]
  36. On spinal noradrenaline receptor supersensitivity: correlation between nerve terminal densities and flexor reflexes various times after intracisternal 6-hydroxydopamine. Nygren, L.G., Olson, L. Brain Res. (1976) [Pubmed]
  37. A method for provoking EEG abnormalities by administration of nialamide. Tanio, M., Shimoda, Y. Folia psychiatrica et neurologica japonica. (1977) [Pubmed]
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