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At least 433 records · Page 24Linked to original sources

PubMed1984

Effect of ovarian steroids on the metabolism of noradrenaline in rabbit uterus.

The metabolism of (-)-3H-noradrenaline was examined in uterine slices from ovariectomized rabbits which were either untreated or treated with 17 beta-oestradiol, alone or in combination with progesterone. 17 beta-oestradiol caused uterine enlargement which was not accompanied by a change in the formation per g of O-methylated metabolites (3H-NMN, 3H-VMA, 3H-MOPEG). Accumulation of unchanged 3H-noradrenaline and the formation of deaminated catechols (3H-DOMA and 3H-DOPEG) were decreased per g tissue, but increased per uterine horn. Progesterone produced further enlargement of the oestrogen-dominated uteri which was accompanied by (a) a decrease in deaminated catechol formation and (b) an increase in 3H-NMN formation per unit mass of tissue. In all uteri (control and hormone-treated), cocaine inhibited the formation of deaminated catechols, but not that of the O-methylated metabolites. It is suggested, therefore, that, per unit of uterine mass, the neuronal deamination of (-)-3H-noradrenaline is decreased by 17 beta-oestradiol and further decreased by progesterone, and that these changes reflect failure of the intraneuronal deaminating system in the whole uterus to increase in proportion to the increase in uterine mass. Since other agents which decreased the deamination of (-)-3H-noradrenaline (cocaine and nialamide) did not affect 3H-NMN formation in oestrogen-dominated uteri, it is suggested that stimulation of 3H-NMN formation represents a direct effect of progesterone on the extraneuronal O-methylation of noradrenaline.

Animals↗

PubMed1985

Immunohistological studies of masked indoleamine cells in the area postrema of the rat.

Masked indoleamine cells (MICS) in the area postrema and adjacent areas in the rat were immunohistochemically studied (the peroxidase-antiperoxidase method) using a serotonin antiserum. After pretreatment with nialamide (200-300 mg/kg), immunoreactive MICS could be observed. They were small cells (about 12 micron in diameter) with several processes and were distributed in nearly all parts of the area postrema and also in the nucleus tructus solitarii. Following a single intraventricular injection of 75 micrograms 5,6-dihydroxytryptamine, the immunoreactivity of these cells conspicuously decreased for several days. The submicroscopical structure of the cells was investigated using immunoelectron microscopy. Immunoreactive products were observed in the cytoplasm as particles with a diameter of 25-40 nm and high electron density, but these were not found in the nucleus or cell organelles.

5,6-Dihydroxytryptamine↗

PubMedDate not supplied

Influence of some monoamine oxidase inhibitors on the sleep-wakefulness cycle of the cat.

The influence of some monoamine oxidase inhibitors (phenelzine, transamin [tranylcypromine], nialamide) on the structure of the sleep-wakefulness cycle of the cat was studied. It was shown that these monoamine oxidase inhibitors elicit and increase in slow-wave sleep in the sleep-wakefulness cycle due to complete suppression of paradoxical sleep and significant decrease in wakefulness. After the cessation of the action of the monoamine oxidase inhibitors, a selective rebound of wakefulness is observed against the background of complete or partial absence of paradoxical sleep. The gives grounds for the hypothesis that during partial deprivation of wakefulness under the influence of monoamine oxidase inhibitors an intensification occurs on the accumulation of specific need for this physiological state, the satisfaction of which is accomplished as the result of its rebound in the post-deprivational cycle, i.e., after the termination of the EEG of the synchronizing effect of the monoamine oxidase inhibitors.

Animals↗

PubMed1977

Localization of 5-hydroxytryptamine and protein(s) in the secretion granules of the rudimentary photoreceptor cells in the pineal of Lacerta.

In order to localize 5-hydroxytryptamine (5-HT) stores, the pineal organ of Lacerta was examined by electron microscopy following argentaffin and chromaffin reactions. The results obtained with these ultracytochemical reactions were correlated with those obtained previously using the Falck and Hillarp method and electron microscopic radioautography. The secretion granules (diameter: 60-340 nm) of the secretory rudimentary photoreceptor (SRP) cells are the locus of the argentaffin and chromaffin reactions. The reactivity of the granules disappeared after p-CPA or reserpine administration and increased after nialamide injection. From the previous and present results it can be concluded that 5-HT in the pineal organ of Lacerta is stored in the secretion granules of SRP cells and coexists with a proteinaceous and/or possibly a glycoproteinaceous component. Whether this secretion is neurohormonal in nature is still not clear.

Animals↗

PubMed1975

Monoamine oxidase inhibitors: nature of their interaction with rabbit pancreatic islets to alter insluin secretion.

Using an in vitro rabbit pancreas system, we studied the effect of monoamine oxidase (MAO) inhibitors on flucose-stimulated insulin secretion. We evaluated the effect of both brief (15 min) and prolonged (60 min) exposure of pancreas segments to non-hydrazine (harmine, alpha-methyltryptamine, tranylcypromine and pargyline) and hydrazine (phenelzine, nialamide, iproniazid) type MAO inhibitors. All of the hydrazine type MAO inhibitors potentiated glucose-stimulated insulin secretion. Of the non-hydrazine inhibitors, only harmine and alpha-methyltryptamine potentiated glucose-stimulated insulin secretion. Hydrazine, although not itself an MAO inhibitor, also potentiated insulin secretion. Sixty minutes of exposure to tranylcypromine or alpha-methyltryptamine caused a decrease in insulin secretion. These MAO inhibitors are primary amines and primary amines can inhibit insulin secretion. The dopamine (DA) or serotonin (5-HT) content of the B-cells was increased by incubating rabbit pancreas with L-3, 4-dihydroxyphenylalanine (L-Dopa) or 5-hydroxytryptophan (5-HTP) for forty-five minutes prior to stimulation with glucose. Non-hydrazine MAO inhibitors increased dopamine inhibition of insulin secretion and either did not alter, or decreased serotonin inhibition of insulin secretion. Rabbit pancreatic islets were isolated using the collagenase digestion technique. The MAO activity of islet homogenates was determined using 5-HT and DA as substrates. Rabbit islet MAO has only one-tenth the specific activity against 5-HT (35 +/- 8.7 mumumoles/mg/min, M +/- SEM) that it has against DA (357 +/- 62.3 mumumoles/mg/min). This suggests that one reason that MAT inhibitors do not increase serotonin inhibition of insulin secretion is because MAO is not the major pathway for 5-HT inactivation in rabbit pancreatic islets. These studies suggest that MAO inhibitors alter insulin secretion, by both decreasing B-cell monoamine degradation and by mechanisms that do not involve MAO inhibition.

5-Hydroxytryptophan↗

PubMed1975

Degenerative processes after punctate intracerebral administration of 6-hydroxydopamine.

Various doses of the neurotoxin 6-hydroxydopamine (6-OHDA) were infused into the substantia nigra-ventromedial tegmental area, caudateputamen nucleus, and red nucleus. A maximum of four successively occurring zones of neuropathology could by detected at all injection sites: (1) A zone of complete absence of neural, glial, and vascular elements due to tissue displacement by the cannula, (2) an area of glial cells, developing over time, which surrounded the cannula tract, (3) a region exhibiting virtually complete loss of neuronal elements, and (4) a zone of selective neuropathological reaction or cellular loss in which some neurons were affected and others were not. All investigators who have histochemically and/or histologically evaluated the effects of intracerebrally administered 6-OHDA agree on the existence and genesis, some non-selective process, of the first three zones. Although some scientists maintain that the fourth zone is where 6-OHDA operates selectively, data are presented in this report that other, well-established processes can account for neuropathology beyond zone 3. Prominent among these are retrograde and anterograde degeneration, ischemia as a function of interruption of blood supply, and nonselective traumatization. In addition, the topography of the injected site (e.g., morphology of affected neurons, degree of myelination) was found to be as important a determinant of the locus of tissue damage as the presumed selectivity of 6-OHDA's action. Furthermore, monoamine oxidase inhibition by nialamide did not appear to increase the neurotoxicity of 6-OHDA. Similarly, 1-(2,5-dihydroxy-4-methylphenyl)-2-aminopropane was not a more potent cytotoxin than 6-OHDA even though this new neurotoxin has a propane side chain which renders it immune to monoamine oxidase. These observations, taken together, suggest that considerable cautioon should be exercised in interpreting data from experiments in which 6-OHDA, or related neurotoxins, are used to uncover catecholaminergic mechanisms of behavior and other functional processes.

Acetylcholinesterase↗

PubMed1981

Reserpine prevents goldthioglucose hypothalamic lesions in mice.

In reserpinized mice the occurrence of goldthioglucose hypothalamic lesions was significantly lower than in control mice. Some protection was also conferred by serotonin-receptor blockers and by treatment with nialamide + DL-alpha-methyldopa, but the protective effect of reserpine was not reversed by serotonergic and dopaminergic agonists, alone or in combination, nor by insulin.

Animals↗

PubMed1981

Comparative studies of the effects of 5-hydroxytryptamine and noradrenaline on the rat anococcygeus muscle.

The effects of 5-hydroxytryptamine (5HT) and noradrenaline (NA) have been studied on rat anococcygeus muscle. 1. 5HT and NA produced a dose-dependent contraction of rat anococcygeus muscle. Cyproheptadine (1.0 X 10(-6) M), a specific 5HT receptor blocker, failed to inhibit the responses to either 5HT or NA. 2. However, phentolamine, a specific alpha receptor antagonist competitively blocked the responses to 5HT and NA. 3. The responses to 5HT were inhibited in the reserpinized (5 mg/kg i.p. 24 h) and 6-hydroxydopamine (6-OHDA) pre-treated preparations. 6-OHDA produced a leftward shift of the dose-response curve of NA. Reserpine pre-treatment potentiated lower doses of NA and the threshold dose of NA was significantly decreased. 4. Nialamide (2.2 x 10(-6) M), the mono-amine oxidase inhibitor produced a significant leftward shift of the dose-response curve of both 5HT and NA. Pyrogallol (2.3 x 10(-5) M), the catechol-o-methyl transferase inhibitor also potentiated the responses to both 5HT and NA, but the potentiation was significant at lower doses of 5HT and NA. 5. Our data suggest that 5HT- and NA-induced contractions in rat anococcygeus muscle are mediated through common alpha adrenoceptors. 5HT actions are probably indirect, mediated through the release of NA.

Animals↗

PubMed1977

Demonstration of a tryptaminergic mechanism in the rat beta-cell.

Yellow 5-HT fluorescence has been histochemically demonstrated in rat pancreatic islet cells in animals injected with L-5-HTP with or without pretreatment with the monoaminoxidase inhibitor nialamide. This fluorescence was not observed after inhibition of the aromatic amino acid decarobxylase. The results strongly suggest the presence of a tryptaminergic mechanism in the rat islet cells.

Benserazide↗

PubMed1990

Gangliosides enhance the anti-immobility response elicited by several antidepressant treatments in mice.

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. Gangliosides, which had no effect per se, showed a clear dose-response relationship in enhancing the anti-immobility effect of desipramine. These results suggest that, regardless of their mechanisms of action, gangliosides facilitate the behavioral response of several antidepressant treatments.

Animals↗

PubMed1996

Exogenous gaseous superoxide potentiates the antinociceptive effect of opioid analgesic agents.

The study examined the potentiation of the antinociceptive action of opioid analgesics produced by gaseous superoxide (GS) in the rat hind paw withdrawal test (PWT) and by GS or hydrogen peroxide (HP) in the formalin test. In the PWT, inhalation of GS for 50 minutes before i.p. injection of threshold doses of morphine (0.5 mg/kg) and trimeperidine (1.0 mg/kg) increased the threshold of nociception (TN) by a maximum of 43.0% (p < 0.05) and 113.4% (p < 0.01) respectively. The GS/trimeperidine-dependent increase in TN showed two peaks, the second of which could be suppressed by nialamide. Naloxone abolished the GS/ morphine-dependent increased in the TN. In the formalin test, a significant antinociceptive effect developed after GS inhalation or HP administration (intranasally, 2 x 5 microliters of 2 x 10(-5) mol/l solution in saline) in combination with low doses of Omnopon (0.06-0.75 mg/kg). These results suggest that both GS and HP potentiate the antinociceptive effects of opioid analgesics.

Analgesics, Opioid↗

PubMed1996

Ultrastructural localization of sympathetic axons in experimental rat sciatic nerve neuromas.

The ultrastructural localization of sympathetic axons was investigated in normal rat sciatic nerves and experimental sciatic nerve neuromas. The best ultrastructural localization of noradrenaline in the dense-cored vesicles of sympathetic axons was accomplished following pretreatment of rats with nialamide and 5-hydroxy dopamine, followed by fixation according to the modified chromaffin technique of Tranzer and Richards (1976). After such preparation, sympathetic axons containing 5-hydroxy dopamine-labelled dense-cored vesicles could be identified in normal sciatic nerve. Large accumulations of labelled dense-cored vesicles were also found in acute neuromas, up to 1 week after nerve section. Much smaller numbers of dense-cored vesicles could be identified in chronic neuromas from 2 to 3 weeks following nerve section. Sympathetic axons could also be identified following electron probe X-ray microanalysis of the tissue sections, using chromium detection as the marker for the noradrenaline-containing dense-cored vesicles. Unusual configurations of Schwann cell subunits, which enclosed myelinated fibres and sympathetic axon sprouts within the same basal lamina, were identified in the acute neuromas, 3-7 days after nerve section. Such configurations may be of relevance to the pathophysiological interaction which develops between sympathetic efferent and sensory fibres in peripheral nerve neuromas.

Adrenergic Fibers↗

PubMed1976

A comparison of cell proliferation in normal and neoplastic intestinal epithelia following either biogenic amine depletion or monoamine oxidase inhibition.

Epithelial cell proliferation was studied in the jejunum and in the colon of normal rats, in the colon of dimethylhydrazine-treated rats and in dimethylhydrazine-induced adenocarcinoma of the colon using a stathmokinetic technique. Estimates of cell proliferation rates in these four tissues were then repeated in animals which had been depleted of biogenic animes by treatment with reserpine and in animals whose monoamine oxidase was inhibited by treatment with nialamide. In amine-depleted animals cell proliferation essentially ceased in all four tissues examined. Inhibition of monoamine oxidase did not significantly influence cell proliferation in nonmalignant tissues but accelerated cell division in colonic tumours.

Adenocarcinoma↗

PubMed1987

Studies on the activity of L-threo-3,4-dihydroxyphenylserine (L-DOPS) as a catecholamine precursor in the brain. Comparison with that of L-dopa.

L-Threo-3,4-dihydroxyphenylserine (L-DOPS) was compared with L-3,4-dihydroxyphenylalanine (L-DOPA) with respect to their activities as central amine precursors. The apparent Km value (the substrate affinity) of L-DOPS for aromatic L-amino acid decarboxylase was nearly equal to that of L-DOPA, whereas the vmax value (the rate of decarboxylation) of L-DOPS was much smaller than that of L-DOPA, the penetration of L-DOPS into the brain through the blood-brain barrier was found to be smaller (about one-fourth) than that of L-DOPA but, for an amine precursor, it was still substantial. Unlike L-DOPA, L-DOPS did not cause a marked accumulation of norepinephrine (NE), the corresponding catecholamine in the brain, but nialamide, a monoamine oxidase inhibitor significantly enhanced the L-DOPS-induced rise of NE. Moreover, the brain concentration of 3-methoxy-4-hydroxy-phenylethyleneglycol (MHPG), the principal end metabolite of NE, was increased markedly by L-DOPS. These results suggest that L-DOPS may act as an NE precursor in the brain and activate NE neurons by increasing the turnover rate of NE.

Animals↗

PubMed1976

Decrease of uptake and exchange of neurotransmitter amino acids after depletion of their synaptosomal pools.

Synaptosomes prelabeled at 37 degrees C with radioactive amino acids (GABA, glutamate, glycine, taurine, alpha-aminoisobutyric acid, phenylalanine, leucine) and then washed at 0 degrees C on Millipore filters (DAWP 02500) lost 60-70% of the accumulated radioactivity. The loss was similar with exogenous tritiated GABA and glutamate, and with [14C]GABA and [14C]glutamate metabolically derived from [14C]glucose. In contrast, radioactive norepinephrine, dopamine and 5-hydroxytryptamine were almost totally retained by cold shocked synaptosomes. After pretreatment with reserpine and nialamide the loss of norepinephrine became significantly greater (about 25%). The uptake of radioactive GABA, glutamate and clycine after cold shock was about 50% reduced, whereas that of radioactive biogenic amines was less affected (reduction of 22% for norepinephrine, 29% for 5-hydroxytryptamine and 35% for dopamine). The loss of amino acids and the reduction of uptake could be minimized by performing the cold shock in hypertonic conditions. In synaptosomes prelabeled with [3H]GABA, a good correlation was observed among magnitude of amino acid pool depletion induced by cold shock or by 56 mM KCl, decrease of subsequent accumulation of [14C]GABA, and decrease of [14C]-GABA-stimulated [3H]GABA release (homoexchange).

Amino Acids↗

PubMed1980

A scanning microfluorimetric study on sympathetic nerve fibres: intraneuronal differences in noradrenaline turnover.

The quantitative aspects of formaldehyde induced fluorescence (FIF) of noradrenaline (NA) in sympathetic nerve fibres were studied in whole mount preparations of the iris of the rat. Both "static" and scanning microfluorimetric measurements showed a close linear relationship between the FIF intensity and the NA content after pharmacological treatment (alpha-methyl-p-tyrosine, amphetamine, guanethidine, nialamide). A histogram analysis method is described to study fluorescence changes in different parts of the nerve fibre histogram, in order to evaluate changes in different segments of the nerve fibres characterized by their fluorescence intensity. The method is illustrated by a study on NA turnover. The chemically determined halflife (T 1/2 of NA after alpha-methyl-p-tyrosine (4.3 h) was in close agreement with the T 1/2 estimated microfluorimetrically (4.2 h). However, pronounced differences were found in various parts of the nerve fibre histogram (3.7-6.3 h). We conclude that the turnover of NA is different in various segments of the sympathetic nerve fibres in the rat iris and that the most intensely fluorescent varicosities display the longest T 1/2 and the highest turnover rate of NA.

Adrenergic Fibers↗

PubMed1981

The effect of 4-aminopyridine on the spinal locomotor rhythm induced by L-DOPA.

In high spinal curarized cats rhythmic motor output similar to locomotion ('fictive locomotion') of all 4 limbs was obtained after intravenous application of the noradrenergic precursor, L-DOPA, and nialamide combined with 4-aminopyridine (4-AP). The activity was recorded from muscle nerves. In the presence of 4-AP, which enhances transmission at various excitatory and inhibitory synapses, reduced amounts of DOPA were sufficient to evoke fictive locomotion. 4-AP alone did not elicit locomotion. The burst rate increased up to 6 Hz with the amount of 4-AP given (0.5-50 mg/kg). The cyclic frequency of high spinal cats exhibiting either fictive locomotion or walking on a treadmill was accelerated by 4-AP. After a supplementary transection of the spinal cord at the upper lumbar level both fore- and hindlimbs generally continued to show fictive locomotion with similar frequencies. In the presence of high doses of clonidine (alpha-receptor-activator, greater than 4 mg/kg), the locomotor pattern was replaced by regular (2 Hz) synchronous discharges in all flexors and extensors.

4-Aminopyridine↗

PubMed1990

Phase-dependent modulation of primary afferent depolarization in single cutaneous primary afferents evoked by peripheral stimulation during fictive locomotion in the cat.

Previous results from our laboratory have shown with intra-axonal recordings that hindfoot cutaneous primary afferents are subjected to rhythmic depolarizations during fictive locomotion (L-PAD) suggesting that cutaneous presynaptic mechanisms are activated by the central locomotor program. In this study, we examined the transmission in pathways responsible for primary afferent depolarizations (PAD) of cutaneous fibres during spontaneous fictive locomotion in decorticate cats and in spinal cats injected with nialamide and L-DOPA. PADs were evoked (E-PADs) by electrical stimulation of peripheral nerves and recorded intra-axonally with micropipettes in identified superficialis peroneal (SP; n = 7) and tibialis posterior (TP; n = 17) cutaneous primary afferents. Results showed that the amplitude of E-PADs, which were superimposed on the L-PAD, was deeply modulated throughout the locomotor cycle; decreasing to reach a minimum during the flexor phase and increasing to a maximum during the extensor phase. The results were not statistically different in fibres of the two nerves and in both types of preparation. The amplitude of E-PADs was always maximum during the extensor phase whether there was a large L-PAD or not during that phase. This suggests that the presynaptic mechanisms activated by central locomotor networks (L-PAD) and those activated by peripheral inputs (E-PAD) may in part be controlled differently. The results thus show that the transmission in PAD pathways activated by cutaneous inputs is phasically modulated by the central pattern generator for locomotion. This strongly suggests that the presynaptic inhibition in cutaneous fibres evoked by the movement-related feedback during real locomotion could be similarly modulated.

Animals↗