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PubMed1981

Inhibition of monoamine oxidase activity after combined action of chlordimeform with the antidepressant nialamide.

The 40-day oral administration of 5, 10, and 50 mg/kg chlordimeform to male rats moderately decreased monoamine oxidase activity (MAO) in the brain, liver, and serum, determined with the substrates kynuramine, tyramine, tryptamine, serotonin, dopamine, and benzylamine. The enzyme was inhibited predominantly in the liver. The study of MAO inhibition after 10 days application of 2, 6, 10, 15, and 20 mg/kg nialamide revealed that 2 mg/kg had a threshold effect. A dose of 6 mg/kg resulted in a pronounced decrease in the enzyme activity. Experiments with a 30-day application of 5, 10 and 50 mg/kg chlordimeform were made, followed by treatment with 6 mg/kg nialamide in combination for another 10 days. The statistical evaluation by the Student's t-test demonstrated increased MAO inhibitory action. Dose-effect relationship was established with kynuramine in liver, brain, and serum, and with benzylamine in liver.

Amidines↗
PubMed1992

Nialamide, an MAO inhibitor, increases urinary excretion of endogenously produced bufotenin in man.

Nialamide, an MAO inhibitor, was given per os (PO) to a normal man who volunteered in two separate trials (total intake 300 mg and 1000 mg, respectively), and his bufotenin excretion was followed by consecutive urine samples. In both experiments the excretion rose well above the values measured from the same test subject when not taking nialamide (median 0.089 nmol/mmol creatinine, range 0.002-1.78). At its highest, the excretion was 16.5 nmol/mmol creatinine, and the maximum urinary output was 495 nmoles (56 micrograms) in 24 hr. The levels of bufotenin in plasma required for the excretion of the latter amounts are not far from those that produce psychic symptoms in man.

Administration, Oral↗
PubMed1987

Chronic administration of desipramine or nialamide decreases wet-dog shakes in rats produced by the TRH-analog MK-771.

The effect of chronic administration of the tricyclic antidepressant, desipramine, or the monoamine oxidase inhibitor (MAOI), nialamide, on the ability of the TRH analog, MK-771, to induce wet-dog shakes in rats was examined. MK-771 at a dose of 3 mg/kg produced significantly fewer wet-dog shakes in those animals treated repeatedly with either nialamide or DMI in comparison to those animals treated chronically with saline. Acute administration of these antidepressant compounds did not alter the ability of MK-771 to produce wet-dog shakes in rats. The results of these experiments indicate that TRH responsiveness in the CNS is reduced by chronic but not acute antidepressant drug treatment, and suggest that TRH may be involved in antidepressant drug action.

Animals↗
PubMed1975

[Effects of nialamide on brain monoamine consumption and liver glycogen content in rats chronically treated with insulin].

Male rats weighing about 50 g were fed a normal-balanced diet for 100 days during which time i.p. injections of saline solution (2 ml/kg) or insulin (4 IU/kg) and/or nialamide (30 mg/kg) were given every two days. The animals were sacrificed 16 hr after the last injection and the brains and livers were extracted for the measurement of tyramine consumption and liver glycogen deposition. It was found that the decrease of glycogen deposition and tyramine consumption induced by nialamide was inhibited by a simultaneous administration of insulin.

Animals↗
PubMedDate not supplied

The effects of neuroleptics and nialamide on defensive conditoned reflex in rats.

Experiments were carried out on male Wistar rats after development of defensive conditioned relex during 6 weeks of training. In one series of experiments chlorpromazine, haloperidol, pimozide or fluspirilene were used in doses of 0.05, 0.5 and 5.0 mg/kg intraperitoneally. In another series of experiments nialamide was given intraperitoneally in a dose of 140 mg/kg 16--18 hours before administration of one of these neuroleptics. A delay in the time of appearance of the defensive conditioned refex was observed after administration of neuroleptics in all animals. In some rats neuroleptics caused complete disappearance of the conditioned refex as well as the defensive unconditioned refex. 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.

Animals↗
PubMed1975

Effect of nialamide and reserpine on brain free amino acids of rat dependent on and withdrawn from morphine.

The brain free amino acid levels were estimated in rats dependent on and withdrawn from morphine. The effects of nialamide and reserpine on the levels of brain free amino acids were investigated during the development of physical dependence on morphine and after the abrupt withdrawal of morphine. The relationships between brain free amino acid levels, and physical dependence and withdrawal syndrome, the relationships between the degree of the manifestations in abstinence under the effects of nialamide and reserpine, and the changes in brain amino acid levels are discussed.

Amino Acids↗
PubMedDate not supplied

[Effect of nialamide administration on avoidance reactions in rats].

Enhanced level of dopamine in the brain caused by one-time administration of nialamide (125 mg/kg into the stomach) does not change the spontaneous motor activity, but increases the number of errors during elaboration of avoidance reaction and during its reversal (changing the side of reinforcement). The rise of the noradrenaline level in the brain, observed after 2 and 3 nialamide administrations does not change parameters of conditioning, but leads to an increase in spontaneous motor activity.

Animals↗
PubMed1981

Comparisons of rotamer populations of nialamide, azaperone, and chloroquine in solid state and in solution.

IR and NMR spectroscopy were combined with previously published X-ray crystallographic data to determine the solution conformations of the -(CH2)n- fragments of nialamide, azaperone, and chloroquine. The solution conformation of these compounds then was compared to the solid-state conformation. In addition, the limits of the IR-X-ray method are discussed. This paper shows that a combination of IR, NMR, and X-ray crystallographic data can lead to a complete picture of the conformations available to drugs. In addition, the danger of using solid-state conformational data alone to make pharmacological suggestions is illustrated.

Azaperone↗
PubMed1984

Interactions of non-selective monoamine oxidase inhibitors, tranylcypromine and nialamide, with inhibitors of 5-hydroxytryptamine, dopamine or noradrenaline re-uptake.

Rats pretreated with tranylcypromine and given clomipramine, developed head and body twitches, forelimb flexor-extensor movements and wet dog shakes, phenomena which failed to develop when pretreatment incorporated p-chlorophenylalanine (PCPA) but were unabated when this included alpha-methyl-p-tyrosine (AMPT). Locomotor activity, itself enhanced by tranylcypromine, was further and significantly elevated compared to saline, by clomipramine or imipramine in grouped rats (n = 3) but not in single or paired rats; desipramine lacked such action. This effect of clomipramine was prevented when PCPA was incorporated into the pretreatment and that of imipramine by including PCPA or AMPT. Brain monoamine oxidase (MAO) A inhibition was 92% and that of MAO B, 80%. Cortical hydroxytryptamine (5-HT) and noradrenaline concentrations as well as hypothalamic 5-HT, were significantly elevated by tranylcypromine, as was dopamine in the striatum, nucleus accumbens and tuberculum olfactorium. Hyperthermia developed in tranylcypromine pretreated rats given paroxetine or fluoxetine. Myoclonic phenomena were elicited by paroxetine, fluoxetine, clomipramine or imipramine in nialamide pretreated rats but these were less intense than in rats pretreated with phenelzine or tranylcypromine. Fatalities were fewer than in rats pretreated with tranylcypromine or phenelzine. Brain MAO A inhibition was 92% and that of MAO B, 69%.

Animals↗
PubMed1987

Differential effects of nialamide and clomipramine on serotonin efflux and autoreceptors.

Serotonin (5-HT) activity in vivo and in vitro was evaluated in rats following acute and chronic administration of the antidepressants nialamide (NMD) and clomipramine (CMI). The 5-HT motor syndrome was used as an index of in vivo serotonergic function. In vitro, 3H-5-HT uptake, potassium-evoked 3H-5-HT release and 5-HT autoreceptor activity were evaluated as measures of presynaptic function. Repeated injections of NMD abolished the 5-methoxy-N, N-dimethyltryptamine (5-MeODMT)-induced motor syndrome and the ability of 5-methoxytryptamine (5-MEOT) to attenuate the potassium-evoked release of 3H-5HT. Autoreceptor subsensitivity was associated with a marked increase in basal and potassium-evoked 3H-5-HT release. In contrast, acute NMD, and acute and chronic CMI did not affect the expression of the motor syndrome or alter 3H-HT release or autoreceptor activity. Acute and chronic injections of NMD enhanced 3H-5-HT uptake. The results suggest that the antidepressant efficacy of monoamine oxidase inhibitor (MAOI) antidepressants may be related to their ability to increase endogenous levels of 5-HT and thereby produce a subsensitivity of 5-HT1 type receptors. This subsensitivity is reflected both by attenuation of the motor syndrome and enhanced 5-HT neurotransmission resulting in part from autoreceptor down-regulation.

5-Methoxytryptamine↗
PubMed1991

Serotonin and nialamide differentially regulate survival and growth of cultured serotonin and catecholamine neurons.

In this morphometric analysis of immunoreactive serotonin (5-HT) and tyrosine hydroxylase (TH) neurons in culture, 5-HT and the MAO inhibitor nialamide influenced the survival, cell body size and neurite outgrowth of embryonic day 14 (E14) 5-HT neurons after treatment from 1-3 days in vitro (DIV), but did not significantly affect E14 or E15 TH neurons of either the noradrenergic or dopaminergic phenotype. These treatments had minimal effects on 5-HT neurons derived from E15 embryos. The stimulatory effects of 5-HT on survival and somal growth of E14 5-HT neurons was in contrast to its inhibitory effects on neurite outgrowth, suggesting trophic and inhibitory autoregulation of different cellular compartments of developing 5-HT neurons. The decreased sensitivity of E15 5-HT neurons to these treatments, despite similar viability and growth of these neurons in control cultures, suggests the existence of a critical period for this regulation during the initial period of serotonergic neurogenesis when these neurons are forming the bilateral B4-9 raphe complex. The lack of significant effects of 5-HT on TH neurons suggests differential sensitivities of 5-HT and TH neurons to developmental regulation by this neurotransmitter.

Animals↗
PubMed1977

The influence of hydrazine, phenelzine and nialamide on gluconeogenesis and cell respiration in the perfused guinea-pig liver.

Hydrazine (2 mmol/l) and phenelzine (0.5 mmol/l), which are known to produce hypoglycaemia, inhibit glucose formation from lactate in the perfused guinea-pig liver. The hydrazone formed from pyruvate and phenelzine exerted the same effect at concentrations of only 0.05 mmol/l. It is suggested that the hydrazones are the substances which are effective. All these compounds inhibited pyruvate consumption and decreased CO2 production by the perfused liver which, togeteher with the pattern of hepatic metabolite concentrations, indicate that they diminish pyruvate metabolism. None of them influenced the activities in vitro of pyruvate carboxylase, phosphoenolpyruvate carboxykinase and pyruvate dehydrogenase. The hydrazone compound caused an increase of the ATP/ADP ration at lower concentrations and an opposite effect above 0.5 mmol/l. Nialamide, another hydrazine derivative, also reduced hepatic glucoeogenesis but led to a marked decrease in the hepatic ATP/ADP ratio and liver cell respiration accompanied by a rise in the 3-hydroxybutyrate/acetoacetate ratio.

Animals↗
PubMedDate not supplied

Determination of mepyramine, aminophenazone, nialamide and chloroquine using the deltapj method.

Mepyramine maleate, aminophenazone, nialamide and chloroquine phosphate are examples of compounds which do not fulfil the requirements of the delta A method. By the proper choice of polynomial and wavelengths, the deltapj method has been successfully applied to their determination. The mean percentage recoveries were found to be 100.2 +/- 0.8, 99.6 +/- 0.6, 99.1 +/- 1.7 and 100.4 +/- 1.3, respectively.

Aminopyrine↗
PubMed1977

Influence of Steroidal enzyme inducers on the toxicity of pyrogallol, pargyline and nialamide.

In rats, the toxic manifestations of overdosage with with parcyline (a monoamine oxidase inhibitor) or pyrogallol (a catechol-o-methyltransferase inhibitor) were diminished by treatment with the more potent steroidal (pregnenolone-16alpha-carbonitrile, spironolactone, etc.) or nonsteroidal (phenobarbital) catatoxic substances. Except for significant protection offered by glucocorticoids (triamcinolene, prednisolone acetate) against pargyline, all other pretreatments (progesterone, estradiol, desoxycorticosterone acetate, etc.) either had no influence on or increase the deleterious effects of the two amine inhibitors. Nialamide intoxication was exacerbated by most of these conditioners.

Animals↗
PubMed1996

Rhythmic discharges recorded from tail muscle nerves after injection of nialamide and L-DOPA solution in spinalized cats.

In 22 decapitated and high spinalized cats, rhythmic discharges were recorded from the nerves supplying the tail muscles, m. extensor caudae lateralis (ECL) and m. flexor caudae longus (FCL) after intravenous injection of Nialamide and L-DOPA solution. In 15 out of 22 cats, stable rhythmic discharges were recorded from tail muscle nerves. Two different discharge patterns were observed. The predominant pattern consisted of an alternating activation between left and right tail muscle nerves and a synchronous activation of ECL and FCL nerves on one side. The second pattern consisted of synchronous activity involving all four tail muscle nerves.

Animals↗