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 577 records · Page 32Linked to original sources

Effects of toluene inhalation on brain biogenic amines in the rat.

The effects of toluene exposure on the biogenic amine concentrations in the central nervous system were investigated in the rat. Toluene was administered via inhalation to groups of rats at concentrations of 0, l00, 300, or 1000 ppm. After an 8-h continuous exposure, animals were sacrificed and whole brain concentrations of dopamine (DA), norepinephrine (NE), and 5-hydroxytryptamine (5-HT) were determined. The data indicated a significant increase in whole brain concentrations of DA following the 100-ppm exposure. A regional analysis of DA, NE, and 5-HT concentrations in rats exposed to 1000 ppm of toluene for 8-h indicated a significant increase in DA concentration in the striatum. A significant increase in NE concentrations was detected in the medulla and midbrain while 5-HT concentrations were significantly increase in the cerebellum, medulla, and striatum. The results indicate that toluene action results in elevated concentrations of behaviorally significant neuro-transmitters.

Animals↗

Influence of formamidines on biogenic amine levels in rat brain and plasma.

Biogenic amine levels in samples of whole brain and plasma following treatment of rats with chlordimeform (CDF), its two N-demethyl metabolites (DMC and DDC), p-chloroamphetamine (PCA), and harmaline were separated by high performance liquid chromatography equipped with fluorescence or electrochemical detection systems. At 1 hr following s.c. injection, CDF (200 mg/kg) caused a reduction in levels of norepinephrine (NE), 5-hydroxytryptamine (5-HT), and tyramine (TRM), an increase in dopamine (DA), and no change in levels of beta-phenethylamine (PEA) in samples of whole rat brain, whereas DMC (100 mg/kg) and DDC (25 mg/kg) effected reductions of brain levels of NE, 5-HT, TRM, and PEA with no change in DA. The effect of DMC (100 mg/kg) on NE and DA levels in brain was followed periodically for 24 hr. Following a significant decrease at 1 hr, NE levels increased to a maximum at 12 hr and remained higher than controls throughout the remainder of the 24 hr test period. DA levels increased during the initial 12 hr and remained significantly higher than controls for the remaining 12 hr. The influence of s.c. vs i.p. administration of DMC (100 mg/kg) on brain amine levels was examined. Intraperitoneal treatment generally resulted in lower amine levels in DMC and vehicle treated animals. Differences in treatment effects were similar for all amines except for 5-HT in which s.c. injection produced a slight reduction, while i.p. injection resulted in a two-fold increase.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Age-related changes in brain biogenic monoamines and monoamine oxidase.

In experiments on 2-, 10- and 22-month old rats, it was found that essential age-related changes occurred in the brain level of biogenic monoamines (BMA) and in the monoamine oxidase (MAO) activity. In 22-month old rats the levels of dopamine (DA), noradrenaline (NA) and serotonin (5-HT) markedly declined in most of the brain structures studied. 5-HT significantly decreased in the frontal cortex, striatum and hypothalamus. DA decreased in the cerebral cortex and striatum and NA in the cerebral cortex. However, the NA level in the striatum of 22-month old rats was increased as compared to that in 2-month old rats. In most cases we observed significant differences (a decrease mainly) also in the level of BMA in 22-month old rats as compared to 10-month old rats. The differences, if any, in the BMA levels between 10- and 2-month old rats were less pronounced. The level of 5-hydroxyindole acetic acid (5-HIAA) in the cerebral cortex and striatum of 22-month old rats was significantly higher as compared to that in 2-month old rats. The MAO-T and MAO-A activities in the brain structures studied were significantly higher in 22-month old rats as compared to those in 2-month old rats. The possibility that the age-related changes in brain neurotransmission might be an important element in the neurochemical basis of some behavioral changes in advanced age is considered.

Age Factors↗

Alterations of fetal brain biogenic amine metabolites by maternal ethanol exposure.

1. Pregnant Sprague-Dawley rats treated chronically with ethanol (3 g/kg daily for the last third of pregnancy) had decreased placental weights at birth (ca 23%). 2. Whole fetal brain levels of HVA and 5-HIAA were similarly decreased 32 and 38%, respectively. 3. MHPG levels were also marginally reduced (i.e. 15% decline). 4. In the presence of a potent type A MAO inhibitor (harmaline, 10 mg/kg maternal weight 2 hr before fetal delivery) co-treatment with ethanol was found to result in a 60% elevation of whole fetal brain norepinephrine levels. 5. Other biogenic amines and metabolites were not altered by ethanol treatment.

Animals↗

Changes in brain biogenic monoamines induced by the nootropic drugs adafenoxate and meclofenoxate and by citicholine (experiments on rats).

1. The effects of Adafenoxate (Adf), meclofenoxate (Mf) and citicholine (CCh) administered at a daily dose of 100 mg/kg for 7 days on the levels of noradrenaline (NA), dopamine (DA) and serotonin (5-HT) in the frontal cerebral cortex, striatum, hippocampus and hypothalamus of rats were studied. 2. Adafenoxate increased the NA level in the striatum and decreased it in the hypothalamus; it increased the DA level in the cerebral cortex and hypothalamus and decreased it in the striatum; it increased the 5-HT level in the cerebral cortex and decreased it in the hippocampus. 3. Meclofenoxate decreased the NA level in the cerebral cortex and hypothalamus; it increased the DA level in the hippocampus and hypothalamus and the 5-HT level in the cerebral cortex, striatum, hippocampus and hypothalamus. 4. Citicholine increased the NA level in the cerebral cortex and hypothalamus; it increased the DA level in the striatum and the 5-HT level in the cerebral cortex, striatum and hippocampus. 5. An attempt is made to explain some similarities and differences in the behavioral effects of the drugs tested (and those observed in other studies) by the changes they induce in brain biogenic monoamines.

Animals↗

Age-related changes of the effects of a group of nootropic drugs on the content of rat brain biogenic monoamines.

1. The changes in the levels of brain biogenic monoamines (BMAs) after chronic (7 days) treatment with piracetam, aniracetam and structural analogues of aniracetam (p-H, p-F, p-Cl, p-P and m-D) were studied in young and old rats. 2. An age-related significant decrease in the BMA content was established in old rats. 3. Most of the investigated compounds increased the level of one or other BMA in one or other of the brain structures studied. This elevation was predominantly established in old rats. 4. The present results and those from previous behaviour studies show that elevation of one or more of the BMA levels in one or more brain regions plays a beneficial role in the realization of their effects on the processes of learning and memory.

Aging↗

Effects of nitrendipine and nisoldipine on biogenic amines in discrete areas of rat brain.

1. Biogenic amines and metabolites were determined in discrete brain sections obtained from rats once or repeatedly treated with nitrendipine or nisoldipine. 2. The increase in both the 5-HIAA levels and the 5-HIAA/5-HT ratio suggested that the drugs activated the serotonergic system in various brain areas. 3. Moreover, nisoldipine decreased the HVA content and the HVA/DA ratio in the striatum. 4. This suggested that nisoldipine, but not nitrendipine, inhibited dopaminergic neurotransmission in this brain area. 5. The effects induced by repeated treatment with nitrendipine or nisoldipine were reduced as compared to those caused by a single administration of these drugs. 6. All these facts could be explained on the basis of the pharmacokinetic properties of nitrendipine and nisoldipine and by the ability of these drugs to interact with the brain VSCC.

Animals↗

Comparison among the effects of nifedipine, nimodipine and nisoldipine on the brain biogenic amines of normal or haloperidol treated rats.

1. Previous studies have shown that dihydropyridine calcium antagonists affected the metabolism of the brain biogenic amines more extensively than the non-dihydropyridine ones. The effects of three dihydropyridines (nifedipine, nimodipine or nisoldipine, 0.05-0.10 mmol/kg i.p.) on brain monoamines and metabolites have been evaluated on both normal and haloperidol treated rats. 2. The small changes induced by the drugs on normal rats were markedly increased in the haloperidol treated rats, clearly showing an inhibition of dopaminergic systems. 3. These effects were selective for the striatum and cerebral cortex, with nisoldipine being more effective than nimodipine or nifedipine. 4. The effects of the three drugs on serotonergic systems were similar or more marked on haloperidol treated rats than on normal rats. These effects, showing activation of serotonergic systems, displayed some regional specificity and different potency of the three compounds. Nisoldipine also appeared to be the most effective drug on serotonergic systems. 5. In conclusion nisoldipine, as well as other calcium antagonists, may have a place in the treatment of some mood disorders.

Animals↗

Interaction between dihydropyridine calcium antagonists and morphine on the brain biogenic amines.

1. Nifedipine, nimodipine or nisoldipine, were i.p. administered to normal, morphine treated or morphine abstinent rats in order to study their effects on brain biogenic amines and metabolites. 2. On various brain areas, the compounds studied decreased DOPAC and/or HVA levels, but increased 5-HIAA levels, leaving unchanged DA and 5-HT contents. 3. This suggested that DA turnover was decreased, whereas 5-HT turnover was increased, by inhibition of neuronal calcium influx. 4. Calcium antagonists: (a) further enhanced the effect of morphine on 5-HT turnover, which may involve an indirect inhibition of voltage sensitive calcium channels; (b) antagonized the effects of morphine on DA turnover, which are believed to be mediated by disinhibition of dopaminergic pathways. 5. The dihydropyridine calcium antagonists showed some differences in regional specificity and in profile of effects.

Animals↗

The co-existence of biogenic amines and neuropeptides in the type I cells of the cat carotid body.

The mammalian carotid body consists of preneural type I (glomus) cells synaptically coupled to afferent axon terminals and enveloped by type II (sustentacular) cells. Recent studies indicate the presence of multiple putative neurotransmitters in this arterial chemoreceptor organ. A double-labeling immunocytochemical technique was utilized which allows simultaneous visualization of two neurochemicals in a single cell. The issue of transmitter co-occurrence in type I cells of the cat carotid body was addressed using specific antibodies for seven neurochemical agents: tyrosine hydroxylase, dopamine-beta-hydroxylase, choline acetyltransferase, serotonin, substance P, met-enkephalin and chromogranin. A high degree (greater than 70%) of co-localization was observed for most pairs of markers, indicating the co-existence of multiple neuroactive agents in type I cells of the cat carotid body. The intensity of staining varied greatly among cells but formed a pattern. Thus, for tyrosine hydroxylase and dopamine-beta-hydroxylase, the majority of double-labeled type I cells exhibited equivalently low or high levels of both, while for the neuropeptides unequal levels of the two markers predominated. Neuropeptides also co-existed in type I cells with catecholamine-synthesizing enzymes and with serotonin. The functional significance of such patterns of multiple co-existence involving biogenic amines and neuropeptides is discussed. Our results indicate a high degree of co-occurrence of reaction product for amine-synthesizing enzymes (tyrosine hydroxylase, dopamine-beta-hydroxylase and choline acetyltransferase), the indoleamine serotonin, and the neuropeptides substance P and met-enkephalin.

Animals↗

Effect of amantadine on motility of reserpinized mice as a function of brain biogenic amines and mouse strains.

The effect of amantadine, reserpine or both on locomotor activity and whole brain content of selected biogenic amines and major metabolites was studied as a function of mouse strain. Successive administration of small dose regimens of reserpine, 0.2 mg/kg IP, did not alter motility from corresponding saline control. Administration of amantadine, 100 mg/kg, IP, prior to each of the reserpine treatments produced either stimulation of motor activity in the albino ICR and black C57BL/6 mice or caused inhibition from reserpine in the albino BALB/C and the brown CDF-1 mouse strains. This suggests a genotype strain sensitivity to the amantadine and reserpine interaction on the motor behavior of the mouse. The amantadine treatment did not alter brain dopamine concentration but increased its immediate acid metabolite, 3,4-dihydroxyphenylacetic acid, in the C57BL/6 mice as contrasted with reduction of the same in the BALB/C mouse strain. Both BALB/C and C57BL/6 mice showed changes in brain normetanephrine levels as a consequence of the pharmacologic intervention used which suggest catecholaminergic sensitivity. The only changes produced by the agents studied in brain serotonin or 5-hydroxyindoleacetic acid levels were confined to the BALB/C mouse strain. No changes occurred in brain levels of the compounds measured from corresponding controls in the CDF-1 mice. The results indicate differential sensitivity of the serotonergic and dopaminergic systems to drug-drug interaction studied which appears to be strain dependent.

Amantadine↗

Significance of biogenic amines for opioid-induced locomotor activity in rats.

The effect of the opioid levorphanol on locomotor activity was investigated in rats treated with p-chlorophenylalanine (PCPA) or 6-hydroxydopamine (6-OHDA). Acute oral administration of 10 or 30 mg/kg levorphanol induces a time- and dose-dependent alteration in motility. Ingestion of 10 mg/kg levorphanol in rats with an intact biogenic amine content results in an increase of locomotion for 180 min followed by a longer lasting, small but significant, reduction of motor activity. The course of motility after 30 mg/kg is similar to that after 10 mg/kg, but the initial peak appears after a 3-h delay. In 5-hydroxytryptamine (5-HT)-deficient rats, the first excitation of motility is enhanced and its subsequent depression intensified. After administration 30 mg/kg a general reduction in motor activity occurs. The effect of 10 mg/kg levorphanol after 6-OHDA treatment is on a lower level, similar to that of rats with intact amine content. After 30 mg/kg levorphanol an immediate and longer lasting increase in activity appears. Chronic ingestion of about 40 mg/levorphanol/kg per day enhances the total amount of activity in normal rats as well as in animals with catecholamine (CA) depletion, but not in those treated with PCPA. In all cases, withdrawal of the opioid results in a reduction of activity below that of control levels.

Animals↗

Biogenic amines: their occurrence, biosynthesis and metabolism in the locust, Schistocerca gregaria, by gas chromatography-negative-ion chemical ionisation mass spectrometry.

Extraction-derivatisation techniques have been developed for the unambiguous identification of biogenic amines, and their putative amino acid precursors and metabolites (both major and minor), in single ventral thoracic nerve cords of the locust. Schistocerca gregaria, by the use of gas chromatography-negative-ion chemical ionisation mass spectrometry with selected ion monitoring. In addition the configuration of that enantiomer of p-octopamine present in the thoracid nervous system of the locust was established as R using the chiral derivatisation reagent, (-)-heptafluorobutyrylphenylalanyl chloride.

Acetylation↗

High-performance liquid chromatographic separation of biogenic polyamines using 2-(1-pyrenyl)ethyl chloroformate as a new fluorogenic derivatizing reagent.

The application of a new fluorogenic pre-column derivatizing reagent, 2-(1-pyrenyl)ethyl chloroformate (PEOC), is reported for the separation and detection of biogenic polyamines using column liquid chromatography. The development of the method included the optimization of excitation and emission wavelengths, efficient gradient programming, derivatization temperature, time, and pH. Minimum detection limits, linear ranges, reproducibility, and recovery from analyzed samples were determined. The procedure was applied to hydrolyzed serum samples taken from healthy individuals and cancer patients. Separation of PEOC-derivatized polyamines from the serum hydrolysis by-products was successful and detection limits were more favorable than those previously reported for 9-fluorenyl-methyl chloroformate-derivatized polyamines.

Biogenic Amines↗

The determination of biogenic amines in four strains of the fruit fly Drosophila melanogaster.

A range of biogenic amines were measured in the heads from four strains of Drosophila melanogaster. Quantitation was carried out using gas chromatography-negative ion chemical ionization mass spectrometry (GC-NICIMS) with stable isotope dilution. The principal amines detected in the heads were dopamine, noradrenaline and 5 HT with small amounts of p- and m-tyramine; p-octopamine could not be detected in samples of 25 heads with a limit of detection of 10 pg per sample. In addition to conventional neurotransmitters or putative neurotransmitters the amines 5- and 6-hydroxydopamine were detected in the heads in substantial amounts.

Animals↗

4-(6-methoxy-2-naphthyl)-2-butyl chloroformate enantiomers: new reagents for the enantiospecific analysis of amino compounds in biogenic matrices.

(+)- and (-)-4-(6-methoxy-2-naphthyl)-2-butyl chloroformate (NAB-C) were prepared from the prochiral non-steroidal anti-inflammatory agent nabumetone with the aim of developing easily detectable chloroformate reagents for the enantiospecific HPLC analysis of amino compounds in biogenic matrices on achiral stationary phases. The new reagents were tested in the derivatization of beta-adrenoceptor antagonists and anti-arrhythmic agents and allowed derivatization in the presence of water. (+)- and (-)-NAB-C were compared with other reagents with a 6-methoxy-2-naphthyl moiety as a chromophore. The reagents were suitable for the analysis of nanogram amounts of, for example, metoprolol enantiomers in plasma, a prerequisite for application in pharmaco- or toxicokinetic studies.

Adrenergic beta-Antagonists↗

Modulating effects of biogenic amines on calcium and ethanol-induced sleeping time.

The present study was carried out in order to clarify the mechanism of calcium prolongation of ethanol-induced sleep. p-Chlorophenylalanine (PCPA, 300 mg/kg), alpha-methyltyrosine (alpha MPT, 100 mg/kg) and diethyldithiocarbamate (DDC, 250 mg/kg) were administered intraperitoneally (IP) to mice to reduce the levels of serotonin (5-HT), dopamine (DA) and norepinephrine (NE) respectively in the brain. Sleeping time was then measured following the administration of ethanol (4.5 g/kg, IP) both with and without CaCl2 (20 mumol/kg, intravenous (IV)). When saline (IP) plus CaCl2 (IV) was administered, the duration of ethanol-induced sleep was prolonged by 100% as compared with saline (IP) plus saline (IV). Duration of ethanol-induced sleep was not changed by PCPA, alpha MPT and DDC. On the other hand, the prolongation of ethanol-induced sleep by CaCl2 was antagonized by PCPA, alpha MPT and DDC. Also, only the DA level in the cerebrum was increased by 25% by administration of CaCl2. We suggest that the increase in ethanol-induced sleeping time due to CaCl2 results from the increase in biogenic amines in the brain.

Animals↗

The effects of some putative transmitters and biogenic amines on uropod abductor muscle in the crayfish Procambarus clarkii and Cambaroides japonicus.

The effects of some putative transmitters and biogenic amines were examined on the uropod ventral abductor exopodite (AbdExV) muscle in two crayfish species Procambarus clarkii and Cambaroides japonicus. Bath application of L-glutamate to the AbdExV muscle caused sustained contract while gamma-aminobutyric acid (GABA) depressed the nerve-evoked contraction of the muscle. Acetylcholine (ACh) had no effect on both the resting tension and the nerve-evoked contraction. Iontophoresis of L-glutamate and GABA onto the surface of the muscle fiber further confirmed that glutamate and GABA are the possible excitatory and inhibitory transmitters respectively at the neuromuscular junction of AbdExV muscle. Bath application of 5-hydroxytryptamine (5-HT) and octopamine (Oct) caused enhancement of the nerve-evoked contraction but dopamine (DA) had no effect on both the resting tension and the nerve-evoked contraction.

Action Potentials↗