Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Biogen”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 379 records · Page 21Linked to original sources
PubMedDate not supplied

Brain biogenic amine levels after methanol administration: possible mechanism of action on central monoaminergic neurons in discrete areas of brain in Wistar rat.

Alterations in the steady state level of rat brain biogenic amines - dopamine, nor-epinephrine, epinephrine, serotonin and 5-hydroxy indole acetic acid, in response to intraperitoneal administration of methanol (3g/kg b.w.) were studied in discrete areas of the rat brain. The monoamine changes induced by methanol were quite different from those induced by ethanol consumption. They were also region-specific; hypothalamus being more vulnerable for methanol-induced monoamine changes. The effects produced by methanol were correlated with the blood and brain level of methanol at the given time, suggesting that the effects were dependent upon the local concentration of methanol in different brain regions. Acidosis induced by ammonium chloride and sodium formate administration did not alter the monoamine levels and therefore, the effects of methanol were not possibly due to acidosis. Blocking or delaying the metabolism of methanol either by 4-Methyl Pyrazole and 3-Amino 1,2,4-Triazole or by simultaneous administration of ethanol resulted in the potentiation of methanol effect. Therefore, it was concluded that methanol induced changes in brain biogenic amines were due to methanol per se and not due to metabolic end products viz. formaldehyde or formic acid.

Acidosis↗
PubMed1988

Effects of the nootropic agents adafenoxate and meclofenoxate on brain biogenic monoamines in aged rats.

The effect of the nootropic agents meclofenoxate (Mf) and adafenoxate (Adf) on the content of biogenic monoamines in the frontal cerebral cortex, striatum, hypothalamus, and hippocampus of 22-month-old rats was studied. Mf and Adf were administered orally for seven days twice daily in a dose of 50 mg/kg weight. Both agents tested increased the content of serotonin (5-HT) in the cortex and striatum. Adf also raised the noradrenaline (NA) content in the cortex and hippocampus, lowering the dopamine (DA) level in the striatum. Comparison of the results obtained in the present study with the finding of earlier experiments of ours on 4-5-month-old rats revealed the following: 1. Biogenic monoamines (BMA) in the brain tend to decrease with ageing. 2. In addition to the unidirectional effects of Mf and Adf on the BMA content in the brain of both young and old rats, but in some cases there were also differences. 3. The comparison of the effects of Mf and Adf on the BMA content in the different brain regions with the changes in this content, characteristic of certain diseases, reveals prospects for selectivity in the application of these nootropic agents, which are generally rather similar in pharmacological characteristics.

Aging↗
PubMed1977

Demonstration of biogenic amines and adrenergic innervation in uveal malignant melanomas by the histoflurometric method.

Clinical and histologic studies were performed on 25 patients with malignant melanomas of the ciliary body and choroid. Portions of fresh tumor were quick frozen and processed by the histofluorometric technique to demonstrate the presence of biogenic amines. Separate portions of each tumor were fixed and processed for routine light microscopy. Specific fluorescence was visible in 21 of 23 pigmented neoplasms. Catecholamine-induced fluorescence of biogenic amines was related to tumor cell type. In two amelanotic tumors no specific fluorescence was seen.

Adult↗
PubMed1988

Identification of nonserotonergic [3H]ketanserin binding sites associated with nerve terminals in rat brain and with platelets; relation with release of biogenic amine metabolites induced by ketanserin- and tetrabenazine-like drugs.

In mammalian striatal tissue and cat platelets, [3H]ketanserin labels besides serotonin-S2 receptors nonserotonergic saturable binding sites. The sites have been distinguished and characterized in [3H]ketanserin binding assays by selective inhibition with tetrabenazine (Ki = 4 nM), a monoamine depleting agent. In rats, the nonserotonergic ketanserin sites were enriched in the striatum (KD = 12.4 +/- 0.3 nM, maximal number of binding sites = 53.2 +/- 11.8 fmol/mg of tissue at pH 7.7, 37 degrees C) and nucleus accumbens. The sites were decreased by 65 to 78% after 6-hydroxydopamine lesions, suggesting an association with dopaminergic nerve terminals. In in vitro superfusion experiments using [3H]dopamine, [3H]norepinephrine and [3H]serotonin loaded rat brain tissue and [3H]serotonin loaded human platelets, 5 min superfusion with 10(-6) M ketanserin, tetrabenazine and reserpine caused instantaneously a marked increase in tritium efflux. The effect was attenuated by the monoamine oxidase inhibitor, pargyline, in brain slices but not in platelets. High-performance liquid chromatography analysis of endogenous catecholamines, serotonin and metabolites in superfusates from striatal slices revealed that stimulation with these drugs provoked mainly release of 3,4-dihydroxybenzeneacetic acid, homovanillic acid, and 5-hydroxyindoleacetic acid. Potencies of a series of ketanserin derivatives, benzoquinolizine derivatives and a variety of drugs affecting neurotransmission were assessed in the in vitro release test using [3H]dopamine loaded striatal slices, and in [3H]ketanserin binding assays to nonserotonergic sites in the striatum and to serotonin-S2 receptors in brain tissue. Activities of drugs in the release test correlated strongly with their binding affinities for nonserotonergic ketanserin sites (rs = 0.83, n = 30, P less than .001). High potency in the latter two tests was confined to few close structural congeners of ketanserin and tetrabenazine. Distinct structural activity relationships for interaction with nonserotonergic ketanserin sites and serotonin-S2 receptors were found. It was concluded that nonserotonergic ketanserin sites mediate release of oxidated metabolites of biogenic amines from nerve endings and of serotonin from platelets. Hence release of biogenic amine metabolites or of cytoplasmic amines is probably not a mere diffusion process but involves specific membranous molecules. Unlike tetrabenazine, ketanserin caused no obvious depletion of central catecholamine and indoleamine stores. Implications of these findings for the mechanism of action of the drugs are discussed.

Animals↗
PubMed1985

[Biogenic amine content of brain sections, blood and adrenals of rabbits exposed to vibration and noise].

Phasic changes of biogenic amines were revealed in brain structures after isolated action of vibration; 15-min vibration increased the content of catecholamines in the hypothalamus and decreased the content of serotonin. 30-min vibration decreased the amount of biogenic amines in the hypothalamus and the cortex. Vibration of a longer duration (1 hr) increased the amount of catecholamines in the brain. After 2-hr vibration the content of catecholamines returned to the control level but the concentration of serotonin still remained above it. Combined action of vibration and noise (2 hrs) decreased the content of catecholamines and increased the amount of serotonin in cerebral structures. Dopamine and serotonin tended to decrease in the blood and adrenals whereas in the urine their amount increased. Multiple combined action of vibration and noise induced the most obvious changes.

Adrenal Glands↗
PubMedDate not supplied

[Effect of 7-hydroxygluacine on brain biogenic monoamines].

In experiments on male albino rats it was established that the aporphine alkaloid 7-hydroxyglaucine injected i.p. at a dose of 1/10 of the LD50 induced many changes in the brain level of biogenic amines. Serotonin content was significantly increased in all brain structures studied (whole brain. cortex, striatum, and hypothalamus) Dopamine level was increased in the whole brain and cortex and was decreased in the hypothalamus; noradrenaline level was increased in the cortex and was decreased in the whole brain and hypothalamus. These effects are thought to be due to the 7-hydroxyglaucine-facilitated transport of amino acids, precursors of biogenic amines, and to neurotransmitter interactions in the different brain structures.

Animals↗
PubMedDate not supplied

[Change in the biogenic amine content in rats in acute and chronic alcohol poisoning].

In Wister line rats subject to determination were the epinphrine, norepinephrine, DOPA, dophamine, serotonin conents and monaminoxidase activity in the blood, liver and brain in acute alcohol poisoning. Acute alcohol poisoning did not produce any substantial changes in the content of biogenic amines in the blood, liver and brain of the rats. With chronic poisoning the content of catecholamines, serotonin increased while the monaminoxidase activity in the study organs declined, this bearing witness to the effect of alcohol on the metabolism of biogenic amines.

Adrenal Glands↗
PubMed1980

Microiontophoresis of biogenic amines on cortical neurons: amounts of NA, DA and 5-HT ejected, compared with tissue content.

The present series of studies were carried out to quantify the amounts of dopamine (DA), noradrenaline (NA) and serotonin (5-HT) ejected from iontophoresis micropipettes and that produce inhibitory and modulatory effects on cortical neurons, in the frontoparietal cortex of the rat and in the occipital cortex of the cat. Using radioactive isotopes of the biogenic amines the effective transport number (n) was found to be 0.08 for DA; 0.13 for NA, and 0.22 for 5-HT. In addition, similar determinations were made, for comparison purposes, of the transport numbers of the neurotransmitters acetylcholine (ACh; n = 0.44), gamma-amino-n-butyrate (GABA, n = 13), and glutamate (GLU; n = 0.27). The quantities ejected under in vivo conditions were then estimated using Faraday's formula and fell in the pmol range (10(-12) mol). The effects of DA, NA and 5-HT on cortical units were studied; the amounts ejected were compared with the endogenous tissue content of these amines, determined by means of specific and sensitive radioenzymatic assays in the regions where the microiontophoretic experiments were performed. These results are discussed in the light of the anatomical, biochemical and electrophysiological data suggesting a modulatory role for the biogenic amines in the cerebral neocortex.

Acetylcholine↗
PubMedDate not supplied

[Inhibition of gamma-amylase of the rabbit liver by biogenic amines and products of their oxidative deamination].

Products of oxidative deamination of biogenic amines (aldehydes) exhibited an inhibitory effect on rabbit liver gamma-amylase activity. The aldehydes, formed after serotonin and 2-phenylethylamine oxidation, proved to be most effective in these systems. Dopamine, noradrenaline and tyramine also caused a slight inhibitory action under these conditions. Biogenic amines and corresponding aldehydes participate apparently in regulation of gamma-amylolysis of glycogen in human and animal organisms.

Animals↗
PubMed1984

[Tissue concentrations of biogenic amines in brain tumors and their distribution].

In recent years, considerable interest has been directed towards the role of neurotransmitters in various types of brain dysfunctions. There are increasing experimental and clinical evidences that disturbances in the metabolism of central monoamine play an important role in the pathogenesis of brain diseases. Brain tumors are thought to affect and change the neurotransmitter function of the surrounding cerebral tissues. In this study, we tried to analyze and accumulate data about tissue concentrations of biogenic amines in brain tumors and their distribution. Samples from thirty-four intracranial tumors removed at operations were studied. The concentrations in tumor tissues were measured by high performance liquid chromatography systems which were equipped with electrochemical detection (LCEC) and were particularly well suited for the separation and the measurement of the concentration of norepinephrine (NE), dopamine (DA), 5-hydroxytryptamine (5-HT), and their metabolites; homovanillic acid (HVA), 5-hydroxyindolacetic acid (5-HIAA) and 3-methyoxy-4-hydroxyphenylethyleneglycol (MHPG) in brain tissues. NE levels were under 3ng/g in twenty-five of thirty cases. DA levels were not detected in more than half of the cases. 5-HT levels varied from 0 ng/g to 166.4 ng/g. HVA levels were detected in one glioblastoma, one metastatic tumor, one meningioma and one hemangioblastoma. 5HIAA levels were not detected in most cases except for two meningiomas and one malignant lymphoma. Distribution of tissue concentrations of biogenic amines and their metabolites in four demarcated brain tumors was studied. Samples for determination of tissue concentrations were taken from tumor tissue at central, middle, and peripheral or adjacent portion from the edge of tumor.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

[Disruption of the regulation of glycogen phosphorylation by biogenic amines].

In rats with experimental cardiomyopathy the content of liver glycogen was considerably higher than in controls and the biogenic amines had no activating effect on glycogen phosphorolysis. The activity of monoamine oxidase was lower in experimental animals than in controls. After injections of monoamine oxidase inhibitors to normal rats no activation of phosphorolysis by biogenic amines was observed.

Animals↗
PubMed1984

Changes in the brain biogenic monoamines of rats, induced by piracetam and aniracetam.

Single oral dose of 600 mg/kg weight piracetam, respectively 50 mg/kg aniracetam, causes essential changes in the level and turnover of dopamine (DA) and serotonin (5-HT) in some rat cerebral structures. When the animals were killed one hour after the administration of the drugs, piracetam significantly increased the DA level in the cerebral cortex and in the striatum, as well as the 5-HT level in the cortex, reducing the 5-HT level in the striatum, brain stem and hypothalamus. At the same time, under the effect of piracetam the DA turnover was accelerated in the cortex and hypothalamus and delayed in the striatum, the noradrenaline turnover was accelerated in the brain stem, the 5-HT turnover was accelerated in the cortex and delayed in the striatum, stem and hypothalamus. Under the effect of aniracetam the DA level was reduced in the striatum and hypothalamus; the 5-HT level was also decreased in the hypothalamus and increased in the cortex and striatum. Aniracetam delayed the DA turnover in the striatum and the 5-HT turnover in the hypothalamus, accelerating the 5-HT turnover in the cortex, striatum and stem. The results obtained show that the changes induced in the cerebral biogenic monoamines participate in the mechanism of action of piracetam and aniracetam, whereby it seems that the analogies and differences in their effects on the cerebral biogenic monoamines play a definite role for the observed analogies and differences in the behavioural effects of these two "nootropic" compounds.

Animals↗
PubMed1981

Comparative histochemistry as a springboard for the discovery of biogenic amines and active peptides in molluscan tissues and amphibian skin.

Histochemistry has been the springboard for the identification in molluscan tissues (hypobranchial body and salivary glands) and amphibian skin of a number of biogenic amines, choline esters and active peptides. Among the biogenic amines 5-HT and related indolealkylamines, octopamine, tyramine and several histamines are to be listed; among the choline esters murexine, dihydromurexine, senecioylcholine and acryloylcholine; among the peptides an array of compounds belonging to at least ten different peptide families. 5-HT, octopamine, tyramine and histamine are present, together with representatives of some peptide families in the posterior salivary glands of octopods, the hypobranchial body of prosobranchiate molluscs and the amphibian skin. This points to the possible occurrence in the above structures of cells belonging to the Pearse's APUD series, intended in its broadest sense. Immunocytochemical studies and even ultrastructural studies on amine and peptide storing cells in molluscan tissues and amphibian skin are virtually lacking. This is certainly a gap that deserves to be filled, considering that these studies may help in elucidating problems of general relevance in invertebrates and vertebrates.

Amphibian Proteins↗
PubMedDate not supplied

Liquid chromatographic method for determination of biogenic amines in fish and fish products.

A liquid chromatographic method with postcolumn derivatization is described for determination of biogenic amines in fish and fish products. Histamine, tyramine, serotonin, beta-phenylethylamine, tryptamine, putrescine, cadaverine, agmatine, spermine, and spermidine can be determined in less than 60 min. Routine sample preinjection treatment implies only 2 extractions with 0.6N perchloric acid and filtration through a 0.45 micron filter. Lack of interferences from volatile amines, amino acids, and dipeptides was verified. Results of reliability study were satisfactory. The proposed method was linear for each amine between 0.25 and 8.00 mg/L. Average recoveries ranged from 92 to 103%. Precisions (coefficients of variation) ranged from 0.70 to 9.75%. Determination limits were < or = 1 mg/kg. A modification in LC conditions was necessary to apply the method to ripened fish products to avoid interferences from food matrixes. In addition, stability of biogenic amines in fresh anchovies and hake during short-term frozen storage was studied. Results showed that, except for agmatine, frozen storage is suitable for keeping samples before analysis.

Alkanesulfonic Acids↗
PubMed1995

Biogenic amine flux mediated by cloned transporters stably expressed in cultured cell lines: amphetamine specificity for inhibition and efflux.

LLC-PK1 cells have been stably transfected with cDNAs encoding the human norepinephrine transporter (NET), rat dopamine transporter (DAT), and rat serotonin transporter. Using these cell lines, the specificity of each transporter toward agents that inhibit substrate influx and stimulate substrate efflux across the plasma membrane was examined. With 1-methyl-4-phenylpyridinium as a substrate for DAT and NET and serotonin as a substrate for the serotonin transporter, each transporter demonstrated a distinct pattern of inhibition by a panel of amphetamine derivatives and analogs, including amphetamine, methamphetamine (also known as "ecstasy"), p-chloroamphetamine, 3,4-methylenedioxymethamphetamine, methylphenidate (ritalin), and 5-methoxy-6-methyl-2-aminoindan. For each cell line expressing a single biogenic amine transporter, efflux of the accumulated substrate was stimulated by amphetamine derivatives, and this efflux was blocked by mazindol, an inhibitor of all three transporters. Of the amphetamine derivatives tested, some caused efflux at concentrations similar to those that inhibited transport. Other derivatives were much less effective at stimulating efflux than at inhibiting uptake. Methylphenidate caused little or no efflux, although it blocked uptake mediated by both NET and DAT. Other inhibitors of transport, such as cocaine, mazindol, citalopram, and nisoxetine, failed to stimulate efflux from these cells at concentrations that inhibited influx. The results suggest that potency toward individual plasma membrane biogenic amine transporters and the ability to release accumulated amine substrates are independent properties of each amphetamine derivative.

1-Methyl-4-phenylpyridinium↗
PubMedDate not supplied

[The morphofunctional heterogeneity between peritoneal and alveolar macrophages in their biogenic amine content: the effect of their presence or absence in the microenvironment of mast cells].

Peritoneal macrophages differ from alveolar ones in biogenic amine content: peritoneal macrophages contain smaller amounts of histamine and serotonin. When activated, alveolar macrophages release biogenic amines, whereas in peritoneal macrophages stimulators of macrophage activity induce the increase in amine content. This may be due to the presence of mast cells in their microenvironment macrophage activity.

Animals↗