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At least 505 records · Page 28Linked to original sources
PubMed1983

Functional development of adrenergic uptake mechanisms in the human fetal heart.

The uptake of 3H-NA into human fetal heart tissue was low during the first half of gestation, only one-fifth of that observed in the mouse heart. A gradual increase in uptake was seen during the second trimester of gestation. A drop in temperature resulted in inhibition of 3H-NA uptake in all samples, but most distinctly in the mouse heart and in the human fetal heart at 14-20 weeks of gestation. Cocaine and desipramine reduced the uptake of 3H-NA in human fetal atria after 14 weeks of gestation but not before that. Nialamide showed no such effect. The functional development of the noradrenergic nervous system in the human fetal heart was found to be very slight during the first trimester of pregnancy. After that a gradual maturation of noradrenergic mechanisms was seen. At the end of the first half of gestation the noradrenergic neurons in the human fetal heart may be held to function qualitatively similarly to those in the mature mouse heart.

Animals↗
PubMed1976

Uptake and metabolism of serotonin by rat adrenal tissue in vitro.

After incubation of separate zones of rat adrenals with radioactively labelled serotonin--at concentrations at which the amine had been previously shown to stimulate aldosterone biosynthesis--the tissue radioactivity was several times higher in the capsular ("zona glomerulosa") than in the decapsulated portions of the glands. High doses of unlabelled serotonin diminished the accumulation of radioactivity, but only when added simultaneously with the tracer. In the course of the incubation, radioactive 5-hydroxy-3-indoleacetic acid, i.e. the deaminated metabolite of serotonin, rapidly appeared in the medium. Most of the radioactive material accumulated by the adrenal was recovered in the cytosol fraction and was no longer identical with serotonin, but consisted mainly of 5-hydroxy-3-indoleacetic acid and another, unidentified metabolite. Unaltered serotonin was found in capsular adrenal tissue extracts only when a monoamine oxidase inhibitor (nialamide) has been added to the incubation medium. Rapid uptake and metabolism thus appeared to be the predominant features of the interaction of incubated adrenal tissue with serotonin. These events may have obscured the possible binding of very small amounts of serotonin to receptor sites. The observed accumulation of radioactivity in adrenal tissue was mainly due to delayed outflow of intracellulary formed metabolite, since 5-hydroxy-3indoleacetic acid was neither taken up by incubated adreanls nor bound by adrenal cytosol. No evidence of serotonin storage in the zona glomerulosa was found in these studies.

Adrenal Glands↗
PubMed1975

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.

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. Injection of the solvent (0-9% isotonic NaCl solution) at the same stage of gestation produced the same but less frequent disturbances. When the rats were injected on days 19 or 21, impairment was less marked than on day 20. Therefore, day 20 seems to be a critical period for the onset of parturition. Injection of Ringer solution into the uterus on day 20 had effects analogous to those of saline injection at the same stage. Anaesthesia induced with ether, laparotomy of the pregnant rat on day 20, and handling of the uterine horns without injection of either Ringer or NaCl also disturbed parturition in 70% of the rats treated. Nevertheless, disorders were not as severe as those after injection. Laparotomy alone on day 20 did not disturb parturition. The effects on parturition of a saline injection into the uterus on day 20 were greatly decreased when the injection was performed on pregnant rats adrenalectomized on day 14, or on pregnant rats pretreated on days 18 and 19 with an agent blocking the adrenergic beta receptors (propranolol); 70-80% of the treated rats had normal deliveries. In control rats, uterine catecholamine levels were markedly modified between days 21 and 22 of gestation. These changes did not occur in rats injected with MAO inhibitor or saline.

Adrenalectomy↗
PubMed1980

Ultrastructural and histochemical studies on the taste buds in some reptiles.

The taste buds in tortoises (Clemmys japonica and Geoclemys reevesii), lizards (Takydromus tachydromoides) and snakes (Elaphe quadrivirgata) were examined by both ultrastructural and histochemical methods. The taste buds consisted of at least three types of cells: the type I, II and III cells. The type I cells were characterized by the presence of secretory dense granules containing polysaccharides which were demonstrated by periodic acid-chromic acid-silver methenamine technique. The type II cells contained numerous tubular, vesicular and lamellated structures. The type III cells were characterized by dense cored vesicles and afferent synaptic contacts. Besides these cells, basally located cells which resembled the basal cells of other lower vertebrates were sometimes found in the tortoises. After administration of L-DOPA following nialamide, some taste bud cells of the tortoises, Clemmys japonica, showed weak yellowish green fluorescence by monoamine fluorescence histochemistry and the dense-cored vesicles in the type III cells increased in number. Acetylcholine esterase activity was not observed in tortoise taste buds. It is suggested that the three types of cells which compose the taste buds of the reptiles may correspond to the three types of cells in mammalian, and the type III cells represent the gustatory cells which are able to potentially produce biogenic monoamines. From these results, the taste buds of the reptiles may hold an intermediate position between those of mammals and amphibia or fishes.

5-Hydroxytryptophan↗
PubMed1978

[Analysis of the circadian rhythm of motor activity in white rats by using several pharmacologic agents which act on cerebral monoamines].

Three pharmacological agents, (disulfiram, imipramine and reserpine) influencing the brain monoamine transmitters have been studied to explain the mechanism involved in the motor circadian rhythm. The new results corroborate our previous ones : the norepinephrine transmitter responsible for the paradoxical sleep is unable to explain the depressed metabolic phase of the circadian rhythm; the negative results obtained with disulfiram and imipramine corroborate the previous results with nialamide. On the contrary, the agents which reduce the serotonine transmitter mechanisms (p-chlorophenylalanine) decrease the difference between active and sleep phases by their action involved in the non-activated sleep. Reserpine, supposed to reduce both transmitter mechanisms (serotonine and norepinephrine) shows a p-chlorophenylalanine-like effect, perhaps more strong. It thus appears that the non-activated sleep is responsible for the two essential sleep functions : the restitution function and the depressed phase of the circadian rhythm.

Animals↗
PubMed1976

Studies on the mechanisms of 6-hydroxydopamine cytotoxicity.

The uptake-accumulation and binding of radioactivity in mouse heart after administration of the catecholamine neurotoxin [3H]6-hydroxydopamine (6-OH-DA, 1 or 3 mg/kg, i.v.) has been investigated. It was confirmed that a substantial portion (8--20%) of the radioactivity taken up and retained by the heart could not be extracted with perchloric acid, in all probability representing covalently bound oxidation products of 6-OH-DA to tissue proteins. Pharmacological analysis showed that a large part of this fraction was associated with the adrenergic nerves. The time-course of the perchloric acid resistant binding to the adrenergic nerves was found to parallel that of the neurotoxic action of 6-hydroxydopamine as evaluated by monitoring the change in [3H]noradrenaline uptake. Calculation of the intranelronal 6-hydroxydopamine concentration (average) needed to induce degeneration showed it to be in the order of 50 mM. The binding ratio for tritium deriving from [3H]6-OH-DA between the intraneuronal and extraneuronal compartments was found to be 10,000 to 30,000, pointing to a very high neuronal specificity for 6-hydroxydopamine. The 'covalent' binding of oxidation products of [3H]6-OH-DA was considerably reduced after desipramine or 1-phenyl-3(2-thiazolyl)-2-thiourea administration, treatments both known to protect the adrenergic nerves from undergoing degeneration. Conversely it was found that the binding increased during conditions known to potentiate the neurotoxic action of 6-hydroxydopamine, e.g., after monoamine oxidase inhibition with nialamide. Subcellular fractionation studies indicated that the predominant site of interaction between 6-hydroxydopamine oxidation products and neuronal proteins is the cytoplasm and the axonal membrane. Analysis of the effect in vivo administration of 6-hydroxydopamine on the field-stimulated induced release of [3H]noradrenaline previously taken up in the adrenergic nerves showed a 6-hydroxydopamine indiced reduction in [3H]noradrenaline release which was approximately proportional to the reduction in the number of nerve terminals. These findings further support the view that 6-hydroxydopamine acts largely in an "all-or-none' fashion with respect to the neurodegenerative action. Administration of [3H]dopamine also resulted in a fraction which was not extractable with perchloric acid, although this fraction was very small compared to that found after an equal dose of [3H]6-hydroxydopamine. These data may indicate that oxidation products of dopamine can interact with tissue proteins. From the present results it can be concluded that there is a close relationship between 'covalent' binding of 6-hydroxydopamine oxidation products to neuronal elements and the cytotoxic action of 6-hydroxydopamine, indicating that this binding may play an important role in the neurodegenerative action of 6-hydroxydopamine on catecholamine neurons.

Adrenergic Fibers↗
PubMedDate not supplied

Influence of albumin degradation products (ADP) on the central action of catecholamines.

The influence of ADP on the central action of catecholamines was investigated. ADP abolished the central action of noradrenaline, amphetamine and nialamide. The peptides decreased apomorphine stereotypy and enhanced haloperidol induced catalepsy. These results support our previous suggestions [10-14] that ADP acts on the CNS by antagonizing the action of central catecholamines.

Albumins↗
PubMedDate not supplied

The central action of intraventricularly (ivc) administered propranolol and phentolamine in rat.

Propranolol (100mug) ivc together with phentolamine (60 mug) decreased spontaneous locomotor activity and weakened post-nialamide locomotor activity in rat. When applied separately in the above doses, neither of the two compounds had this action. Depression of amphetamine-induced locomotor activity was observed after propranolol (250 mug) together with phetolamine (60 mug). Phentolamine alone, had hypothermic action but when applied together with propranolol, it increased after 4 hrs body temperature. The tested compounds prolonged hexobarbital-induced sleeping time but did not affect noradrenaline or dopamine levels in rat's brain.

Animals↗
PubMed1975

[Prevention of cerebrovascular disorders with adrenergic substances].

The author suggests an experimental model of cerebrovascular disorders of the neurogenic (adrenergic) nature following the administration of KCl into the lateral ventricles of the brain of cats or dogs. Surgical desympathization considerably reduced the spasms of the cerebral vessels caused by the central effect of KCl. Dihydroergotoxin, phenoxybenzamine, tropaphene, guanethidine and nialamide produced both the therapeutic and the prophylactic influence under the mentioned experimental disorders of the cerebral circulation.

Animals↗
PubMed1975

The effect of antidepressants on the calcium content of the aorta of reserpine-treated rabbits.

The pre-administration of reserpine in a dose of 5 mg/kg b.o. i.v. 24 before the experiment reduced the calcium content of the thoracic aorta of rabbits weighing 1,000--1,500 g. It had no effect on the calcium level in older animals. The calcium content also fell after 10 days' administration of reserpine in daily doses of 0.1 mg/kg b.w. Pre-administration of the monoaminooxidase inhibitors phenelsine and nialamide inhibited the reserpine-induced decrease in the calcium content of the vascular wall, although by themselves they had no effect on it. Prothiadene, a thymoanaleptic, likewise inhibited, the decrease in the calcium content when administered per os in a dose of 5 mg/kg b.w. 5 hours before reserpine.

Animals↗
PubMed1990

[Role of peripheral adrenergic links in the development of antidepressive effect in an experimental model of behavioral depression in rats].

The study was made on the reserpine model of behavioural depression in cats. The morphofunctional state of peripheral adrenergic nerves in control experiments and under action of antidepressants (befol and nialamid) was studied by fluorescent microscopic method. One definite correlation was shown between the state of somatovegetative changes and the level of neuromediator activity of the adrenergic structures. It was established that the used antidepressants (more expressive by befol) have protective effect in depressive conditions.

Adrenergic Fibers↗
PubMed1990

Ultrastructural study of small granule containing (SGC) cells in the lower mesenteric ganglion in drug treated guinea-pigs.

Small granule containing cells (SGC or SIF cells) in the lower mesenteric ganglion of the guinea-pig were studied in control and experimental animals. After reserpine administration a decrease of dense population of granular vesicles was found. After injection of nialamide and dopamine to the animals in SGC cells significantly increased the number and density of granular vesicles. No real efferent synapses were found on SGC cell processes, although sites with accumulated synaptic-like vesicles, mostly with a dense core, were often observed.

Animals↗
PubMed1990

Effect of selective monoamine oxidase A and B inhibitors on footshock induced aggression in paired rats.

Effects of a selective monoamine oxidase (MAO)--A inhibitor, clorgyline, a selective MAO-B inhibitor, deprenyl, and a non-selective MAO inhibitor, nialamide, were investigated on footshock-induced aggression (FIA) in paired rats. The doses and pretreatment times of the inhibitors used were based on an earlier reported in vivo dose-response and time-course study. In addition, apomorphine, a dopaminergic receptor agonist, and beta-phenylethylamine, a preferred substrate for MAO-B, were also used to garner corroborative evidence. The results of the study indicate that selective MAO-A inhibitors are likely to attenuate FIA by augmenting central serotonergic activity, while selective MAO-B inhibitors accentuate the behaviour by facilitating dopaminergic activity. A permissive role for noradrenaline could not be delineated by the available data.

Aggression↗
PubMed1989

[Inhibitory effects of L-threo-DOPS on electroshock seizure in mice].

Effects of L-threo-3,4-dihydroxyphenylserine (L-DOPS), a synthetic norepinephrine (NE) precursor, on electroshock seizure were studied in mice. All substances were administered intraperitoneally. Minimal electroshock seizure threshold (EST) was not significantly altered by L-DOPS at a dose of 200 or 400 mg/kg. L-DOPS was unable to abolish tonic extensions of hind legs in maximal electroshock seizure (MES) test at doses from 100 to 400 mg/kg. However, it significantly reduced extension/flexion (E/F) ratio in a dose-dependent manner. Furthermore, L-DOPS dose-dependently blocked maximal electroconvulsions in a combined use with nialamide (30 mg/kg), desipramine (20 mg/kg) or maprotiline (40 mg/kg) at so small doses as not to show any anticonvulsant effect when they were used alone. ED50 (with 95% confidence limit) of L-DOPS in the combination treatments were 210 (145-305), 160 (100-256) and 95 (50-181) mg/kg respectively. Those results indicate that L-DOPS has an anticonvulsant property, which is potentiated by a MAO inhibitor or NE uptake blockers. It was presumed that the effect of L-DOPS was caused by the inhibition of spreading of seizure discharges. It was suggested that L-DOPS would be a useful substance for the investigation on a role of NE in experimental epilepsy and could be used clinically as an adjunct drug for generalized tonic-clonic convulsions.

Animals↗
PubMed1989

[Antioxidant therapy of purulent wounds in animal experiments].

A new complex method for treating purulent wounds has been elaborated in the experiment on 22 mature chinchilla rabbits with a simulated abscess. It has been established that a combined use of a 2% alcohol solution of ionol, a 10% aqueous solution of urotropin for irrigation of the wound cavity and a single administration of nialamide cuts down the time two-fold for cleaning wounds and development of granulations and by 40% for the wound complete healing.

Animals↗
PubMedDate not supplied

Investigation of some effects of levamisole on dog blood pressure.

The effects of levamisole were investigated on the blood pressure of anaesthetized dog. Levamisole (0.5 to 4.0 mg/kg) elicited a biphasic effect, an initial brief depressor response followed by a pressor response. The pressor response was dose-related and was blocked by phenoxybenzamine. The residual depressor response was blocked by propranolol. Repeated administration of a high dose of levamisole produced tachyphylaxis. The pressor response to levamisole was not modified by either reserpinization, acute bilateral adrenalectomy or pretreatment with cocaine, whereas pretreatment with dexamethasone, nialamide or pyroaallol shifted the dose-response curve to the right. Levamisole potentiated the pressor responses to noradrenaline, angiotensin and acetylcholine. The effects of levamisole are ascribed to inhibition of monoamine oxidase, catechol-O-methyl transferase, catecholamine uptake2 mechanism and cholinesterase.

Adrenalectomy↗
PubMed1987

[Effect of various monoamine oxidase inhibitors on the structure of the sleep-wakefulness cycle of the cat].

The effect of some monoamine oxidase inhibitors (phenelzine, transamine, nialamide) on the structure of the cat sleep--wakefulness cycle involved an increase of slow-wave sleep at the expense of totally inhibited REM sleep and substantial reduction of wakefulness. Following this effect, selective rebound of wakefulness occurred against the background of total or partial absence of REM sleep. The partial deprivation of wakefulness induced with monoamine oxidase inhibitors seem to entail an accumulation of a specific need in the given physiological state, the gratification of which is effected through its rebound in the post-deprivation cycle.

Animals↗