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At least 523 records · Page 29Linked to original sources

PubMed1987

Influence of reserpine on in vivo localization of injected lymph node cells in the mouse.

The effects of reserpine, and other agents that affect the storage and availability of 5-hydroxytryptamine (5HT), on the localization of injected 51Cr-labelled syngeneic lymph node cells have been investigated. A high dose (5 mg/kg) of reserpine to the recipients reduced localization in the lymph nodes and prevented the usual accumulation of lymphocytes in lymph nodes draining the site of an antigen (sheep erythrocytes: SE) injection. These effects were partially reversible by the monoamine oxidase inhibitor nialamide. This dose of reserpine produced deep sedation throughout the period of the experiment. Lower doses, up to 2.5 mg/kg, produced little sedation and had no effect on the localization of lymphocytes. Other workers had previously reported reduced localization of cells in delayed-type hypersensitivity (DTH) lesions after treatment of the recipients with 5 mg/kg reserpine, and had interpreted this in terms of a role of 5HT in promoting vascular permeability and egress of blood cells. The effect of lower doses of reserpine was not reported. We suggest that the effects on cell localization in both sets of experiments may have been secondary to the general state of sedation and not attributable to a direct local influence of 5HT. Other effects of reserpine included prolonged retention of lymphocytes in lungs and blood, and a reduction of cellularity and DNA synthesis in the thymus, spleen and lymph nodes.

Animals↗

PubMedDate not supplied

Short- and long-term effects of intraventricular 6-hydroxydopamine in rats pretreated with a monoamine oxidase inhibitor.

Bilateral intraventricular injections of high dose (2 X 250 microgram) of 6-hydroxydopamine to rats pretreated with nialamide produced a pronounced hyperactivity persisting for several hours and induced permanent aggressiveness. Only 50% rat survived the treatment for longer than a week, the explorative activity of the survivors was inhibited for over 2 months. The brain catecholamine content was depressed for at least 15 months, while no long-term changes of serotonin level were observed. The hyperactivity, aggressiveness and hypothermia produced by apomorphine were enhanced in centrally chemosympathectomized rats, while the hyperactivity produced by D-amphetamine or amantadine remained inaffected. The results confirm the development of dopamine receptor supersensitivity following central chemosympathectomy, and indicate a possibility of employing the supersensitivity model for distinguishing between pre- and postsynaptic action of dopaminergic stimulants.

Aggression↗

PubMed1982

Serotonin-stimulated cyclic AMP synthesis in the rabbit corneal epithelium.

Serotonin increases the level of cyclic AMP in incubated rabbit corneas; the concentration of agonist producing half-maximal stimulation is approximately 1.5 microM. Nialamide, an inhibitor of monoamine oxidase, potentiates the response to serotonin but not to epinephrine. Amitriptyline, an inhibitor of neuronal uptake of serotonin, does not potentiate the stimulation of cyclic AMP synthesis. Lysergic acid diethylamide, but not timolol, antagonizes the response to serotonin; the half-maximal inhibitory concentration is approximately 6 nM lysergic acid diethylamide. A comparison of the time course of the increase in cyclic AMP synthesis after addition of serotonin or epinephrine to the incubation media indicates that serotonin, but not epinephrine, must penetrate a barrier to its free diffusion. We conclude that the corneal epithelium contains specific serotonergic receptors that, upon activation, cause the synthesis of cyclic AMP, which mediates the stimulation of chloride transport (c.f. companion article, Klyce et al.). The serotonergic receptors must be at a location posterior to the beta-adrenergic receptors, which are on the anterior-surface of the apical cells.

1-Methyl-3-isobutylxanthine↗

PubMed1984

[Plea for monoamine oxidase inhibitors. Retrospective study of 350 cases].

The case-records of 350 outpatients treated with monoamine oxidase inhibitors have been reviewed. All patients presented with depression, obsessions or phobias. About two-thirds benefited from the drugs, particularly after other treatments (including psychotropic drugs, seismotherapy, psychotherapy and internment) had failed. With the moderate doses administered (iproniazide: 50 mg/day; nialamide: 100 mg/day) side-effects were uncommon and mild and no incident was noted in 32 general anaesthesias given for surgical operations. These findings should help in lifting the ban on this category of drugs. Monoamine oxidase inhibitors are effective, useful and sometimes indispensable after failure of other antidepressants.

Adult↗

PubMed1978

Clinical investigation of the menstrual cycle. II. Neuroendocrine investigation and therapy of the inadequate luteal phase.

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. Equalization of the lengths of both the follicular phase and the luteal phase to the normal range was observed during the drug therapy. Forty-five per cent of the pregnancy rate was achieved in 36 of the 80 infecund patients within 4 months of treatment. The mode of action of these drugs is still unknown.

Adult↗

PubMed1984

Addition of the effects of norepinephrine and acetazolamide to decrease formation of cerebrospinal fluid.

In a system for ventriculocisternal perfusion of the choroid plexus, the rate of formation of new cerebrospinal fluid was measured by changes in dilution of an impermeant dye in the perfusate. Norepinephrine added to the perfusate decreased formation of cerebrospinal fluid in rats as was previously demonstrated in rabbits. The dose-response relationship for rats was determined. The formation rate was decreased 42% by 10(-3) M norepinephrine. Acetazolamide, 50 mg/kg i.v., caused a decrease of 46%. Given together, these drugs decreased formation 79%, demonstrating essentially full addition between the regulatory mechanisms involved. Addition of equal magnitude occurred when intraventricular nialamide, an inhibitor of monoamine oxidase, and i.v. acetazolamide were given together. This demonstrates addition between acetazolamide and endogenous norepinephrine (or other catecholamines present) in which metabolic breakdown is prevented by the inhibitor. The degree of reduction in cerebrospinal fluid formation seen in these experiments exceeds that reported for numerous other trials of single drugs.

Acetazolamide↗

PubMed1980

Reserpine abolishes movement-correlated atropine-resistant neocortical low voltage fast activity.

Following a large dose of atropine, rats display large amplitude slow waves in the neocortex during immobility, tremor, tooth-chattering and face-washing (Type II behavior) but display low voltage fast activity (LVFA) during walking, struggling, postural changes and head movement (Type I behavior). Rats treated with a large dose of reserpine usually continue to display LVFA during immobility as well as during movement although large amplitude slow waves are present more frequently than normal. A combination of reserpine and atropine abolishes all LVFA even during intense sensory stimulation or electrical stimulation of the reticular formation. Chlorpromazine, lysergic acid diethylamide, methysergide, phenoxybenzamine, pimozide, promethazine, propranolol and trifluoperazine do not have this effect when combined with atropine. In rats treated with nialamide prior to reserpine and atropine, LVFA continues to occur in association with Type I behavior just as in rats given atropine alone. It is proposed that the occurrence of LVFA in the neocortex is determined by two distinct reticulocortical systems. A cholinergic system produces all LVFA occurring during Type II behavior and a second system, dependent on a monoamine, produces LVFA in association with Type I behavior. The view that LVFA is a correlation of arousal or the sleep-waking cycle is criticized.

Animals↗

PubMed1978

Specific characters of serum MAO in dogs.

The effect of Tris-hydroxymethylaminomethane (Tris) on MAO activity in dog serum was studied by a modification of the method of McEwen and Cohen. Partially purified MAO from dog serum was inhibited 75% and 31% by 10 mM and 1 nM Tris, respecitively. The inhibitory effect of Tris was 1/10 of that by nialamide and 1/1000 of that by catron. Tris also slightly inhibited MAO activity in rabbit serum, but did not affect MAO from bovine or human serum, or from dog liver, kidney or brain. The extent of inhibition of dog serum MAO by Tris remained constant during incubation for 3 hrs. The inhibition was found to be reversible and noncompetitive. Benzylamine was most rapidly oxidized by MAO of dog serum followed in order by amylamine, beta- phenylethylamine and tyramine, while tryptamine and serotonin were not oxidized. Tris inhibited MAO activity with benzylamine or butylamine as substrates, but it was scarcely inhibitory with tyramine or beta-phenylethylamine as substrate. This work shows that Tris is a specific inhibitor of dog serum MAO and suggests that dog serum MAO may differ in enzymic properties from MAO in other animals.

Animals↗

PubMed1980

Distribution and fine structure of the interstitial cells of Cajal.

Distribution and fine structure of the interstitial cells of Cajal were studied in the cat's small intestine. They were only found in the circular muscle layer. They had a slender structure with numerous mitochondria, rough endoplasmic reticulum and granular or secretory vesicles 100 to 300 nm in diameter. The closest distance between the membrane of smooth muscle cells and interstitial cells was 40 to 60 nm. Some nerve bundles were found in close relation to their processes, but neither pre- nor postsynaptic differentiation could be observed. After nialamide treatment the quantity of secretory vesicles increased and therefore it is suggested that these cells have a secretory function producing some kind of peptide and so they may act directly on the smooth muscle cells.

Animals↗

PubMedDate not supplied

Stimulatory and inhibitory action of clonidine on the locomotor activity in the rat.

Clonidine depresses "motivated" but stimulates "basal" locomotor activity of normal rats. It does not affect the "dopaminergic", but inhibits "noradrenergic" locomotor stimulation produced by intraventricularly administered L-dopa methyl ester to nialamide-pretreated rats, although it does not affect the brain norepinephrine accumulation observed after administration of the dopa derivative. The importance of experimental protocol and the possible mechanism of "antiadrenergic" action of clonidine are discussed.

Animals↗

PubMed1976

The effect of lithium chloride on the activity of some psychotropic drugs.

LiCl administered for 4 days enhances amphetamine-induced locomotor stimulation, increases amphetamine toxicity in aggregated mice but does not affect amphetamine stereotypy. Administered together with nialamide, LiCl increase locomotor activity of mice and rats. The administration of this compound together with reserpine reverses central effects of its action (hypothermia, decreased motility, enhancement of hexobarbital activity).

Amphetamines↗

PubMed1976

Histochemical mapping of dopamine neurons and fiber pathways in dog mesencephalon.

A topographic mapping of dopamine (DA)-containing neurons and fibers was done mainly in the mesencephalon of the dog using the fluorescent histochemical technique of Falck and Hillarp. The extensive DA neuron system was found to be located in the ventral and medial regions of the mesencephalon; the pars compacta of the substantia nigra, the area almost corresponding to the ventral tegmental area of Tsai (which consists of three groups, a caudal, the nucleus parabrachialis pigmentosus, a ventral, the nucleus paranigralis and a rostral, the caudal part of the nucleus tegmentalis ventralis of Tsai), the nucleus linearis of the raphe, and the mesencephalic reticular formation. The nigro-neostriatal projection can be traced in the non-treated or nialamide plus L-dopa treated puppies without the lesion-degeneration technique. Most fibers arising from these DA cell groups assemble at the prerubral area and ascend just dorsal to the medial forebrain bundle. Most fibers turn laterally at the lateral hypothalamus and enter the neostriatum via the dorsal part of the subthalamic nucleus, the zona incerta and the capsula interna. These findings show that the distribution of DA neurons and the nigro-neostriatal pathway are fundamentally similar to those in other mammals. In this study, the processes of the nigral and paranigral DA neurons have been demonstrated to project into the pars reticulata in the dog.

Animals↗

PubMed2000

R-(-)-Deprenyl inhibits monocytic THP-1 cell neurotoxicity independently of monoamine oxidase inhibition.

R-(-)-Deprenyl (deprenyl, selegiline), a monoamine oxidase B (MAO-B) inhibitor, delays progression of Parkinson's disease. This action could be mediated by inhibition of MAO-B but there may also be unrelated mechanisms. Direct neuroprotective and antiapoptotic actions of deprenyl have previously been observed in vitro. Here we describe an antineurotoxic action of deprenyl which is independent of direct neuronal effects. We employed a previously described assay in which human neuroblastoma SH-SY5Y cells are exposed to cell-free supernatants of stimulated human monocytic THP-1 cells. Deprenyl reduced the secretion of neurotoxic products by such stimulated cells in a concentration-dependent manner, while the MAO inhibitors iproniazid, isocarboxazid, nialamide, tranylcypromine, phenelzine, and clorgyline were without effect. No antineurotoxic action was observed when deprenyl was added directly to SH-SY5Y cells. Messenger RNAs for MAO-A and MAO-B were not detected in THP-1 cells by reverse transcriptase-polymerase chain reaction analysis of total RNA extracts. Such mRNAs were easily detected in extracts of SH-SY5Y cells under comparable conditions. MAO enzymatic activity was also undetectable in THP-1 cell lysates, while it was readily observed in SH-SY5Y cells. It was concluded that the effect of deprenyl on THP-1 cells was not mediated by MAO and that deprenyl itself was not protecting neurons. These data suggest that deprenyl may have utility in neurodegenerative diseases due to its antineurotoxic actions.

Alzheimer Disease↗

PubMed1994

Hydralazine and other hydrazine derivatives and the formation of DNA adducts.

Previous work has demonstrated that hydrazine after formylation to its corresponding hydrazone may be activated both in vivo and in vitro to a methylating intermediate resulting in the formation of O6-methyl- and N7-methylguanines in DNA. Incubation of calf thymus DNA with the hydrazine derivative, hydralazine, and formaldehyde resulted in the production of N7-methylguanine and two aberrant bases in DNA. These bases were separated by strong cation-exchange high-performance liquid chromatographic fractionation of neutral thermal hydrolysates. Administration of hydralazine to rats resulted in the formation of N7-methylguanine in liver DNA, but the two unknown bases observed in the in vitro experiment could not be demonstrated in vivo. In contrast to hydrazine, administration of hydralazine resulted in the methylation of DNA only at doses approaching the LD50, suggesting that formylation does not represent a significant mechanism for hydralazine toxicity in the system described. Hydralazine in combination with formaldehyde resulted in the formation of triazolophthalazine, a metabolite which has been characterized in man. The ability of 17 other hydrazine derivatives to alkylate liver DNA was determined after single administration to young adult male Sprague-Dawley rats or C57BL6 mice. Quantifiable amounts of N7-methylguanine were measured in liver DNA from animals treated with 10 of the 17 compounds. In 3 of the 10 cases quantifiable amounts of O6-methylguanine were also measured. Methylation of liver DNA guanine was obtained with hydrazine, hydralazine, procarbazine, isoniazid, phenylhydrazine, nialamide, nitrofurazone, maleic hydrazide, sulfomethoxypyridazine, and sulfamethiazole and two hydrazine-formaldehyde polymerization products, formalazine and tetraformyltrisazine.

Alkylation↗

PubMed1985

Hypothalamic catecholamine histofluorescence in dwarf mice.

Brains of growth hormone (GH)- and prolactin (PRL)-deficient Ames (df/df) and Snell (dw/dw) dwarf mice and normal mice of the same strains were examined for catecholamine (CA) histofluorescence, with particular emphasis upon the hypothalamic tuberoinfundibular (A12) (arcuate nucleus/median eminence) region, which plays a role in the regulation of both GH and PRL. Dwarfs and normal animals of both types also were treated with a drug regimen to deplete sequentially neuronal CA stores (reserpine), inhibit CA oxidation (nialamide) and load dopaminergic A12 cells with exogenous transmitter (norepinephrine), in order to test viability and axonal transport capacity of A12 neurons. In both types of dwarfs, compared with normals, fluorescence was markedly reduced in the zona externa of the median eminence, which is normally rich in terminals from A12 neurons. Fluorescence in the median eminence was particularly weak in Ames dwarfs, and A12 perikarya were difficult to discern in this group. Snell dwarfs showed reduced fluorescence of A12 perikarya when compared with the brightly fluorescent perikarya seen in normal mice. In supraoptic and paraventricular nuclei, and in the zona interna of the median eminence, CA fluorescence attributable to NE was comparable among dwarfs and normals; fluorescence of dopaminergic perikarya in substantia nigra was also unaffected in dwarfs. Exogenously administered NE effected enhanced fluorescence of A12 perikarya in normal mice and in Snell dwarfs; NE treatment in the Ames dwarf, however, failed to increase significantly the faint fluorescence of A12 cell bodies. The results indicate that dopaminergic A12 neurons in Snell dwarf mice are present and viable.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1984

Organ culture of the goldfish pineal body. An ultrastructural and biochemical study.

The ultrastructure and biochemistry of the goldfish pineal organ were examined in explants cultured for 1, 3, and 6 days. All four cell types (photoreceptor, supportive, ganglion, phagocytic) were identified; they exhibited many of the characteristics of these cells in vivo. Exceptions included a gradual disorganization of the outer segments and reduction of synaptic ribbons in photoreceptors with time in culture. In addition, there was a marked proliferation of endoplasmic reticulum in both photoreceptor and supportive cells. The indoles 5-hydroxytryptophan, serotonin, 5-hydroxyindoleacetic acid, 5-methoxytryptophol, and melatonin were separated in explants by high performance liquid chromatography using electrochemical detection. Serotonin levels could be depleted by p-chlorophenylalanine and elevated by nialamide or by adding 5-hydroxytryptophan to the culture medium. These findings suggest that organ culture may be a useful model for study of regulatory processes related to the photoneuroendocrine functions of the teleost pineal organ.

5-Hydroxytryptophan↗

PubMed1975

Histochemical observations on uptake of L-dopa into endocrine cells of the rat pituitary gland during the postnatal development.

The uptake of L-dopa into the cells of the adenohypophysis of the rat was studied during the postnatal development and at adult age using the formaldehyde-induced fluorescence method (FIF). The cells taking up L-dopa were classified by Alcian blue-PAS-Orange G staining. The correlation between the cells taking up L-dopa and those containing tryptophyl-peptide was estimated during the postnatal period and in adult rats. The cells containing tryptophyl-peptide were demonstrated using fluorescence induced by treatment with combined formaldehyde and acetyl chloride vapour. The following observations were made: 1) Great majority of the cells taking up L-dopa did not contain tryptophyl-peptide. Thus the accumulation of L-dopa into the cells of pars distalis is not due to accumulation of L-dopa into the cells by the same transport mechanism as the amino acids for tryptophyl-peptide. 2) Of the cells taking up L-dopa in the adult rats 96% were chromophobes, 2.0% acidophilic cells (somatotrophs and cells producing prolactin), 0.9% R-mucoid cells (corticotrophs), and 1.2% S1- and S2-mucoid cells (gonadotrophs and thyrotrophs). At 10 and 25 days' age the relative numbers of the cells taking up L-dopa were about the same. 3) Pretreatment with nialamide caused only a slight increase in the number of the cells taking up L-dopa. The decrease in the number of the cells uptaking L-dopa of the pars distalis, which takes place after 5 weeks' age is thus not caused by the increased MAO-activity. 4) Strongly chromophilic cells did not take up L-dopa. At the light of our results it seems evident that L-dopa is taken up by the chromophobic cells when these differentiate into chromophilic cells. The accumulation of L-dopa may be a sign of an active transport of amino acids into the cells. The accumulation of L-dopa into the chromophobic stellate and follicular cells may reflect their metabolic activity. These cells probably have an important role in the production of the hormones of the pars distalis.

Adrenocorticotropic Hormone↗

PubMed1976

Postnatal ontogenic development of the adrenergic innervation pattern in the rat portal vein. A histochemical study.

The postnatal development of the adrenergic innervation pattern in the rat portal vein has been studied with the histochemical fluorescence method of Hillarp and Falck. Stretch preparations and transverse freeze-dried sections of intact portal veins were studied from rats during the first 5 weeks of life and from adult rats. Orientation of undifferentiated smooth muscle cells into two layers was observed at 4 days of age. Dominance of the thick outer longitudinal muscle layer was apparent at two weeks of age. A terminal adrenergic nerve plexus with some varicosities was restricted outside the media at the end of the first week. Ingrowth of penetrating non-terminal adrenergic nerve fibers through the longitudinal muscle layer occurred during the second week of age when the main terminal nerve plexus was developing between the two muscle layers. After 3 weeks of age the adult pattern of a two-dimensional adrenergic plexus between the muscle was established. In the adult rat pharmacological treatment with nialamide and noradrenaline revealed the thin, penetrating non-terminal adrenergic nerve fibers in the longitudinal muscle layer which were poorly visible otherwise. The present observations strongly indicate that the main adrenergic plexus between the two muscle layers emanates directly from the outer axonal plexus. These findings are discussed regarding possible trophic interactions between ingrowing sympathetic adrenergic vasomotor nerves and maturing vascular smooth muscle.

Animals↗