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At least 19 recordsLinked to original sources
PubMed1972

On the role of central nervous system catecholamines and 5-hydroxytryptamine in the nialamide-induced behavioural syndrome.

1. Intraperitoneal administration of nialamide, 200 mg/kg, to mice elicited a pronounced increase in motor activity and rectal temperature concomitant with a gradual increase in the concentrations of 5-hydroxytryptamine (5-HT), noradrenaline (NA) and dopamine in the brain.2. In mice treated with L-tryptophan, 300 mg/kg, 1 h before nialamide, the increase in motor activity appeared earlier than after nialamide alone, and the hyperthermia was more pronounced. The increase in 5-HT concentrations in the brain was more pronounced in these animals, whereas the concentrations of NA and dopamine were of the same magnitude as after nialamide alone.3. Treatment with p-chlorophenylalanine methylester-HCl (PCPA), 400 mg/kg, 24 h before nialamide partially antagonized the increase in motor activity and the accumulation of NA and dopamine was not significantly different from that observed after nialamide alone.4. Treatment with PCPA, 800 mg/kg, 72, 48 and 24 h before nialamide, completely antagonized the increase in motor activity and rectal temperature. The accumulation of brain 5-HT was greatly depressed in these animals. The concentrations of dopamine 1, 3 and 6 h and the concentration of NA 6 h after the nialamide injection were significantly lower in the mice given PCPA 800 mg/kg x 3, than in the mice given nialamide alone.5. Administration of DL-5-hydroxytryptophan, 30 mg/kg, 1 h after the nialamide injection, to mice pretreated with PCPA, 800 mg/kg x 3, restored the increase in motor activity and rectal temperature.6. L-Tryptophan, 300 mg/kg, given 1 h before nialamide to mice pretreated with PCPA, 800 mg/kg x 3, elicited a moderate increase in motor activity and a slight increase in the accumulation of 5-HT in the brain when compared to that after PCPA, 800 mg/kg x 3, and nialamide.7. Administration of alpha-methyltyrosine methylester, 200 mg/kg, 2 h before nialamide partially antagonized the increase in motor activity and completely antagonized the increase in rectal temperature elicited by nialamide alone. The accumulation of brain NA and dopamine was inhibited in these animals.8. It is concluded that the excitation in mice, elicited by nialamide, is mediated largely via brain 5-HT, but that also the brain catecholamines seem to contribute to this effect.

5-Hydroxytryptophan↗
PubMed1986

Effect of nialamide on the metabolism of dopamine injected into the nucleus accumbens of old rats.

We have reported previously that after nialamide pretreatment there is an age-related difference in the stimulation of locomotor activity produced by the injection of dopamine bilaterally into the nucleus accumbens. Thus, the stimulation of locomotor activity produced by dopamine in old rats was significantly less than that of young and mature rats. The purpose of the present study was to determine whether nialamide was an effective inhibitor of the metabolism of dopamine after dopamine was injected into the nucleus accumbens of old rats. When we measured the concentration of injected dopamine in the limbic forebrain (nucleus accumbens and olfactory tubercle) of young (6 months), mature (15 months) and old (26 months) rats pretreated with nialamide, the amount of dopamine that was present was significantly less in old rats than in young or mature rats. 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. 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. 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.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1989

Nialamide-induced hypermotility in mice treated with inhibitors of monoamine uptake, 5-HT antagonists and lithium.

When administered orally to mice 1 h before nialamide 100 mg/kg SC two non-selective and nine selective 5-HT uptake inhibitors enhanced the hypermotility produced by nialamide, whereas two inhibitors of NA uptake showed no influence on the nialamide response. Paroxetine was the most potent nialamide potentiator; 100% increase in motility response was obtained at 0.012 mg/kg. 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. Nialamide 100 mg/kg was given SC to groups of mice being treated for 4 weeks with paroxetine and lithium given through the diet. At daily intakes of paroxetine and lithium resulting in therapeutic plasma or serum levels a distinctive nialamide potentiation was found.

Animals↗
PubMed1977

A method for provoking EEG abnormalities by administration of nialamide.

Nialamide, a kind of monoamine oxydase inhibitor, was used for provoking centrencephalic EEG abnormalities and 6-14 Hz positive spikes. It was assumed that these EEG abnormalities have close relationship with dysfunctions of the brainstem which is rich in monoamines and monoamine oxydase. The nialamide provocation was carried out on 49 inpatients who had centrencephalic discharges in their EEG reports. These patients consisted of four cases of epilepsy, one case of anorexia nervosa, two cases of narcolepsy and 42 cases of diencephalosis. Another series of 22 patients suffering from other diseases, in whome EEG no centrencephalic EEG abnormallities were detected, were examined with nialamide. Out of the 49 patients, 35 cases (71.4+) showed increased EEG abnormalities following the administration of nialamide. It was noteworthy that this drug had provocative effect not only for EEG abnormalities, but also for the symptoms from which patients were suffering. In 26 out of 49 patients, both EEG abnormalities and clinical symptoms were provoked by nialamide. And the nialamide administration resulted in negative on all 22 patients who did not register centrencephalic EEG abnormalities. The mechanism and characteristics of this provocative procedure by the use of nialamide were evaluated.

Adult↗
PubMed1989

Promotion by nialamide of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

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. 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. 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. However, it did not affect the histology of the cancers. Nialamide also caused a significant increase in tissue norepinephrine concentrations in the gastric wall and in the labeling indices of the gastric mucosae. However, nialamide had no influence on serum gastrin levels in the fasting state and after re-feeding. These findings indicate that nialamide promotes gastric carcinogenesis and that this may be related to its effects in increasing norepinephrine in the gastric wall and stimulating proliferation of gastric epithelial cells.

Adenocarcinoma↗
PubMed1976

5-Hydroxytryptophan (5-HTP) and a MAOI (nialamide) in the treatment of depressions. A double-blind controlled study.

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). The patients treated with nialamide + l-5-HTP achieved a fuller recovery than those who were treated with nialamide alone. The treatment with nialamide + l-5-HTP proved to have a shorter delay of onset. Side effects showed no marked differences except for the orthostatic hypotension which was less apparent in those patients treated with nialamide + l-5-HTP.

5-Hydroxytryptophan↗
PubMed1985

Locomotor response of nialamide pretreated old rats to intraaccumbens dopamine.

The objective of this study was to determine the locomotor activity response of young (6 month), mature (15 month), and old (26 month) rats to bilateral intraaccumbens injections of dopamine after pretreatment with nialamide. Young and mature rats responded to dopamine with high rates of activity, while old rats either did not respond at all or responded with a lower intensity of activity. In contrast, the response of old rats to dopamine or ergometrine alone or to dopamine after pargyline pretreatment was not less than that of mature and young rats. These results suggest that the attenuated response of old rats to dopamine after nialamide pretreatment is not due to a decrease in dopamine receptor activity, but appears to be due to some unique property of nialamide in these animals. However, the reduced response of old rats to dopamine was not due to the inability of nialamide to inhibit monoamine oxidase, since nialamide completely inhibited the activity of this enzyme in the nucleus accumbens of old rats.

Aging↗
PubMed1987

Influence of an inhibitor of monoaminooxidase (nialamide) on the absorption and retention of nitrogen in adult rats.

A study was made on adult rats (170 g) of the effect of nialamide (20 mg/100 g of diet), an inhibitor of monoaminooxidase, administered for 15 or 30 days (short or long-term, respectively), with food intake controlled (pair fed), on the absorption and retention of nitrogen, and on the nitrogen content in the liver, the gastronemio and longissimus dorsi muscles and in the small intestine. Nialamide administered for a time which can be considered prolonged (30 days) negatively affects absorption of alimentary protein, while metabolic utilization is reduced when the drug is administered both in the short and the long term. Proteic catabolism is less marked in male rats, due to the hormonal anabolizant situation in this sex. Nitrogen content under the effect of nialamide showed no significant variation in the gastronemio muscle or in the small intestine. There is a clear reduction in the longissimus dorsi muscle and an increase in the liver of those animals of both sexes treated with the drug, with the exception of male rats given nialamide in the long term.

Animals↗
PubMed1984

Effects of nialamide on responses of dog isolated arteries to tyramine and transmural electrical stimulation.

In dog mesenteric arteries, nialamide (10(-5) M), a monoamine oxidase inhibitor, potentiated contractile response to tyramine but not to noradrenaline or transmural electrical stimulation (TES). Bretylium, desipramine or prior reserpinization inhibited the potentiating action of nialamide on the tyramine-induced contraction. Contractions induced by octopamine were not reduced by prior reserpinization. In the coronary artery, relaxing responses to tyramine were potentiated but those to noradrenaline and TES were not potentiated by nialamide. In the cerebral artery, nialamide failed to potentiate tyramine-induced contraction. The functional role of intraneuronal monoamine oxidase in sympathomimetic effects is discussed.

Animals↗
PubMed1989

Influence of an inhibitor of monoaminooxidase (nialamide) on the serum levels, urinary excretion and plasma clearance of urea, uric acid and creatinine in adult and growing rats.

Serum levels, urinary excretion and plasma clearance of urea, uric acid and creatinine were studied in adult (230 g) and growing (75 g) rats under the influence of nialamide (an IMAO) administered in daily doses of 20 mg/100 g diet during 15 or 30 days in adults and 10 mg/100 g diet during 15 days in growing rats. A pair feeding design was used in both ages. Serum levels of urea rose in adult rats fed nialamide for 30 days while urinary excretion decreased. No change in serum levels were noted in growing rats although urinary excretion showed a net increase. Serum uric acid levels were increased in adult female rats given nialamide for 30 days, while urinary excretion fell in both sexes. Growing rats showed a drop in urinary excretion of uric acid. Serum creatinine levels were unchanged in adult and growing rats after treatment with nialamide, although a marked increase was recorded in urinary excretion in both groups.

Age Factors↗
PubMed1986

Reversal of the reserpine-induced ptosis by L-threo-3,4-dihydroxy-phenylserine (L-threo-DOPS), a (-)-norepinephrine precursor, and its potentiation by imipramine or nialamide.

The effect of L-threo-DOPS on the reserpine-induced ptosis in mice and its modification by imipramine, a norepinephrine (NE) uptake inhibitor, or nialamide, a monoamineoxidase inhibitor, were studied. Intraperitoneal (i.p.) injection of L-threo-DOPS (800 mg/kg) significantly reduced the severity of the ptosis. This reversal of the ptosis by L-threo-DOPS was markedly potentiated by i.p. injection of either imipramine (2.5 mg/kg) or nialamide (30 mg/kg). Response to L-threo-DOPS was also significantly potentiated by intracerebroventricular (i.c.v.) injection of imipramine (10 micrograms). On the other hand, this treatment with imipramine (10 micrograms, i.c.v.) also significantly potentiated the reversal of the ptosis by NE (20 micrograms, i.c.v.), but the reversal by the subcutaneous (s.c.) injection of NE (1 and 3 mg/kg) was not affected. Reserpine (5 mg/kg, i.p.) markedly decreased the brain content of NE in mice, whereas L-threo-DOPS (400 mg/kg, i.p.) slightly restored it. Moreover, by the pretreatment with nialamide (30 mg/kg, i.p.), L-threo-DOPS produced a significant increase in the brain content of NE in reserpine-treated mice. These results suggested that L-threo-DOPS was capable of reversing the reserpine-induced ptosis due to the formation, at least in part of (-)-NE at the synaptic sites of central noradrenergic neurons.

Animals↗
PubMed1975

Potentiating effect of lithium chloride on aggressive behavior induced in mice by nialamide plus L-DOPA and by clonidine.

Effects of acute administration of LiCl on aggressive behavior and alterations in brain norepinephrine (NE), dopamine (DA) and serotonin (5-HT) contents induced by nialamide plus L-DOPA and by clonidine were examined in mice. Effects of LiCl on turnover and metabolism of brain NE were also investigated. LiCl potentiated the aggressiveness induced by both nialamide plus L-DOPA and by clonidine. Increase in levels of brain NE, DA and 5-HT by nialamide plus L-DOPA was not affected by LiCl. The potentiating effect of LiCl on clonidine aggression was not observed in mice pretreated with disulfiram. Although LiCl did not alter the steady state levels of brain NE, DA and 5-HT, it increased the turnover of NE and decreased the content of endogenous normetanephrine. These results favour the assumption that lithium reduces the ability of nerve terminal vesicles to store NE leading to an increased turnover and decreased concentration of NE at receptor sites.

Aggression↗
PubMed1985

Study of absorption and retention of nitrogen in fast growing rats--II. Influence of IMAO (nialamide).

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). The administration of nialamide reduces the protein absorbed and retained to a significant degree, both in males and females. No difference was observed between the sexes caused by the effect of the drug, due to the absence of the hormonal anabolizant situation caused by testosterone in adult rats. The administration of nialamide does not significantly modify nitrogen content per 100 g of body weight in any of the organs studied, with the exception of the longissimus dorsi.

Animals↗
PubMedDate not supplied

The circadian rhythm of rat motor activity and the effect of brain monoamine inhibitors (PCPA and nialamide).

The study of the circadian motor rhythm in free-running conditions of 500 g rats during 6 successive days shows that the endogenous period of the rhythm in these conditions is 23.40 hrs. The two poisons studied (PCPA in 40 mg/100 g dose and nialamide 5 and 10 mg/100 g doses) have both a deep effect on the functioning of the endogenous rhythm. PCPA reduces the amplitude of the increase of night over day activity to a fourth of the control value. The reducation may be attributed either to increased day activity or to reduced night activity. Nialamide reduces the amplitude of this increase to 80 or 70/100 of control value; this was observed with 5 or 10 mg nialamide/100 g body weight. The most important effect of nialamide on the endogenous rhythm lies in the disappearance of the regular shortening of nearly 20 min of the endogenous rhythm in DD conditions. The abrupt transition for LD 12:12 conditions to DD disturbs the endogenous period for 24 hrs.

Animals↗
PubMed1987

Comparative study of the influence of an inhibitor of monoaminooxidase (nialamide) on the calcium and phosphorus metabolism in slow and fast-growing rats.

Nialamide was supplied to slow-growing animals in doses of 20 mg/100 g of diet for 15 or 30 days. The dose for fast-growing animals was 10 mg/100 g of diet. The digestive utilization of calcium and phosphorus decreases significantly when adult slow-growing rats receive the drug for 30 days. This fall is already important in fast-growing rats when they receive nialamide for only 15 days. In the same way the falls in the retention of calcium and phosphorus in adult rats are only evident when the period of treatment is through 30 days, even females being in negative balance of phosphorus. The amount of calcium retained decreases significantly in fast-growing rats and so does phosphorus impressively after only 15 days of treatment.

Animals↗
PubMed1975

Effects of antagonists upon locomotor stimulation induced by injection of dopamine and Noradrenaline into the nucleus accumbens of nialamide-pretreated rats.

The effects of injections of monoamines, alone and in combination with different antagonists, bilaterally into the nucleus accumbens of nialamide-pretreated rats were investigated. Dopamine was found to produce a stronger stimulation of locomotor activity than noradrenaline, whereas serotonin was effective only in a small number of animals, in which the duration of locomotor stimulation was shorter than after dopamine or noradrenaline. The effects of both dopamine and noradrenaline were completely antagonized by administration of a small dose of the dopamine antagonist haloperidol, administered bilaterally 15 min after the catecholamines. The alpha-adrenergic antagonist phentolamine did not inhibit the effect of noradrenaline but, on the contrary potentiated and considerably prolonged the duration of locomotor stimulation. Aslo, the effect of dopamine was potentiated and prolonged by phentolamine. Bilateral injection of phentolamine alone had no influence upon locomotor activity. The effect of noradrenaline was not clearly inhibited nor potentiated by the beta-adrenergic antagonist propranolol. It is suggested that the stimulation of locomotor activity induced by injection of noradrenaline into the uncleus accumbens of nialamide-pretreated rats is brought about via dopaminergic mechanisms.

Animals↗
PubMed1976

Effect of cortisone, aldosterone and nialamide on "amphetamine stereotypies" and brain methamphetamine levels of adrenalectomized rats.

Cortisone, aldosterone or nialamide was administered to adrenalectomized or sham-operated rats for 7 days, and methamphetamine was injected 24 hrs after the last injection of these compounds. Stereotyped head movement and licking activity were scored 5 min, 30 min and 60 min after methamphetamine injection and, in parallel brain methamphetamine levels in similarly treated rats were measured 5 min, 30 min and 60 min after the methamphetamine injection. Adrenalectomy depressed stereotyped head movements but enhanced the brain amphetamine accumulation. Nialamide but not the hormones further increased the amphetamine accumulation in adrenalectomized rats. No drugs had any effect on the amphetamine-induced head movement suppressed by adrenalectomy.

Adrenal Glands↗
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↗