Effect of some monoamine oxidase inhibitors on deamination of biogenic monoamines by rat liver mitochondrial monoamine oxidase.
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Alkaloids↗
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On the selective inhibition by some monoamine oxidase inhibitors of deamination of biogenic monoamines in vivo.
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Animals↗
Effects of meclofenoxate on the level and turnover of biogenic monoamines in the rat brain.
The level and turnover of biogenic monoamines in some rat brain structures were determined after treatment with meclofenoxate at a dose of 50 mg/kg administered i.p. two times a day (9 a.m. and 5 p.m.) for 5 days. Meclofenoxate decreased dopamine (DA) turnover in the frontal cortex and striatum and highly increased it in the hypothalamus. The DA level significantly declined in the striatum, tended to decline in the cortex and significantly rose in the hypothalamus. The noradrenaline (NA) turnover and level in the cortex and striatum were decreased. Meclofenoxate decreased serotonin (5-HT) turnover in the cortex, striatum and hypothalamus and increased it in the pons. At the same time, the 5-HT level rose in the cortex, striatum and pons and declined in the hypothalamus. These results suggest the neurochemical basis of the psychotropic and neuroendocrine effects of meclofenoxate.
Animals↗
Biogenic monoamines in the freshwater snail, Biomphalaria glabrata: influence of infection by the human blood fluke, Schistosoma mansoni.
The biogenic monoamines, serotonin (5-HT), dopamine (DA) and L-dopa were measured using high performance liquid chromatography with electrochemical detection (HPLC-ED) in the extracts of the central nervous system (CNS) and plasma of uninfected freshwater snails, Biomphalaria glabrata, and in snails at 7, 14, 21 and 28 days postexposure (PE) to the miracidia of the human blood fluke, Schistosoma mansoni. Relative to age-matched uninfected snails, a general depression of biogenic amine levels was observed in the plasma (cell-free haemolymph) and the CNS of infected snails, especially during the latter phase of the prepatency period. Significant decreases were first observed in the CNS of infected snails beginning at Day 14 PE for DA and 5-HT and Day 21 PE for L-dopa. Parasite-exposed snails also exhibited an early and persistent suppression of plasma 5-HT concentrations, starting at 7 days PE and continuing throughout the infection test period. In order to determine the effect of 5-HT on reproduction and, thereby, establish a possible relationship between the observed parasite-induced reduction in 5-HT levels and parasitic castration, the effect of exogenous 5-HT on individual infected and uninfected B. glabrata was investigated. Repeated treatment with 10 microM 5-HT promoted both ovulation and oviposition in B. glabrata. Snails treated with 5-HT consistently layed more eggs than did sham-treated controls. Infected snails that were treated with 5-HT exhibited similar egg-laying rates as those of both serotonin-treated and untreated, uninfected snail groups, thus reversing the castrating effects of larval infection. These findings suggest that 5-HT acts as a stimulant for egg production in B. glabrata, and that parasitic castration may be due, at least in part, to larval-induced suppression of 5-HT in the snail's CNS and plasma during the course of infection with S. mansoni.
Animals↗
[Changes in the balance of biogenic monoamines and their metabolites in the organs of rats with oxygen-induced epilepsy].
The content of some biogenic monoamines and their metabolites in rat brain and heart in different periods of oxygen epilepsia was studied using high performance liquid chromatography with electrochemical detection. It was shown that already at the 5th minute of exposure to oxygen adrenaline, DOPA and some noradrenaline metabolites disappeared in the brain and noradrenaline level reduced. At this period in rat heart the reduction of catecholamine content was the most distinct and serotonin level was unchanged. At the beginning of convulsive period the modifications of biogenic amines content were nonparallel in brain regions: in the heart the reduction of catecholamine level went on, especially in right ventricle. In the terminal phase of oxygen epilepsia brain biogenic amines increased, however, not up to normal meaning, heart catecholamines at this period were at the same level as at the beginning of the convulsive period.
Animals↗
Biogenic monoamine turnover in discrete rat brain regions is correlated with conditioned emotional response and its conditioning history.
The content and turnover of dopamine, norepinephrine and 5-hydroxytryptamine (serotonin), and the content of their respective major metabolites were evaluated in 19 discrete brain areas of rats exposed to conditioned emotional response (CER), and in control groups which received either equivalent yoked shock (shock only) or compound stimulus presentation (tone only). On test day, CER animals suppressed responding and exhibited forms of emotional behavior after presentation of the conditioned stimulus (CS); while shock only and tone only control groups, and CER animals which received an acute dose of diazepam prior to testing, did not suppress. Few changes were observed in content of the biogenic amines or their metabolites, suggesting that the behavioral manipulations were acting within normal physiological limits. On the other hand, numerous changes were observed in the utilization of the 3 biogenic monoamines, which were correlated with the conditioning-anxiety (comparisons of CER vs shock only) and the shock history (comparison of shock only vs tone only). These observations are consistent with putative neural pathways in the frontal cortex, septum, nucleus accumbens, amygdala, striatum, hippocampus and brain stem (which utilize specific monoamines), and with discrete brain areas which have been implicated in classical conditioning and CER-related phenomena. These observations suggest roles for biogenic monoamines in mediating or responding to the classical conditioning and emotional components of the paradigm.
Animals↗
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↗
[The histochemical demonstration of biogenic monoamines in normally developing amphibian embryos and in exposure to a permanent magnetic field].
It was shown that the permanent magnetic fields at 35-40 mT1 inhibit the activity of biogenic monoamines in developing amphibian embryos. The effect was quantitatively similar to that of PMF at 40 mT1 (3-hour exposure during 6 days). The most significant fluctuations in their activity were observed at the stages of blastoderm formation and gastrulation onset.
Amphibians↗
Early postnatal effects of prenatal exposure to glucocorticoids on testosterone metabolism and biogenic monoamines in discrete neuroendocrine regions of the rat brain.
We investigated the effects of hydrocortisone acetate and dexamethasone administered to pregnant rats during the last gestational week on sexual differentiation of testosterone metabolism and biogenic monoamine contents and turnover in the discrete brain regions in 10-day-old offspring. In the preoptic area, sex-dependent differences in aromatase activity were attenuated by prenatal glucocorticoids. Prenatal dexamethasone but not hydrocortisone acetate caused the inversion of sexual dimorphism of 5alpha-reductase activity in the preoptic area. In the brain preoptic area of the male pups prenatally exposed to hydrocortisone acetate, a decrease in noradrenaline turnover was found. Dopamine turnover in the preoptic area and 5-hydroxytryptamine metabolism in the preoptic area and medial basal hypothalamus increased in females as a result of hydrocortisone acetate treatment. Our results indicate that excess glucocorticoids in prenatal life modifies the basic neurochemical and neurophysiological mechanisms of sexual brain differentiation and might contribute to behavioral and reproductive disorders in adulthood.
Animals↗
Effect of preparations from potentiated ethanol on the content of biogenic monoamines and metabolism of ethanol in tissues of rats during alcoholization.
The effect of homeopathically potentiated ethanol (C30 and C200) on ethanol metabolism was studied in alcoholized rats. We measured ethanol concentration in the blood, alcohol dehydrogenase activity in the liver, and contents of biogenic monoamines in the hypothalamus, septum, and whole blood. Potentiated preparations of ethanol were efficient after long-term treatment and delayed ethanol elimination from the blood. Preparation C200 increased alcohol dehydrogenase activity. Potentiated preparations of ethanol (particularly C200) produced a positive effect on catecholaminergic and serotoninergic systems of the brain, i.e. they enhanced protective and adaptive reactions.
Alcohol Dehydrogenase↗
Evaluation of toluene exposure via drinking water on levels of regional brain biogenic monoamines and their metabolites in CD-1 mice.
Toluene, a potentially neurotoxic substance, is found in trace amounts in groundwater. Adult male CD-1 mice were continuously fed drinking water ad libitum containing 0, 17, 80, and 405 mg/liter toluene. After a 28-day treatment, animals were tested for endogenous levels of the biogenic monoamines norepinephrine (NE), dopamine (DA), and serotonin (5-HT) and their respective metabolites. 3-methoxy-4-hydroxymandelic acid (VMA), 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), and 5-hydroxyindoleacetic acid (5-HIAA), in six discrete brain regions. The maximum toluene-induced increases of biogenic amines and their metabolites generally occurred at a toluene concentration of 80 mg/liter. In the hypothalamus, a major NE-containing compartment, the concentrations of NE significantly increased by 51, 63, and 34% in groups dosed with 17, 80, and 405 mg/liter, respectively. Significant increases of NE were also observed in the medulla oblongata and midbrain. Concomitantly, concentrations of VMA increased in various brain regions. Concentrations of DA were significantly higher in the corpus striatum and hypothalamus. Alterations in levels of DA metabolites, DOPAC and HVA, were marginal. Toluene significantly increased concentrations of 5-HT in all dissected brain regions, except cerebellum, and increased the 5-HIAA levels in the hypothalamus, corpus striatum, and cerebral cortex.
Animals↗
[Biogenic monoamines of the brain and spinal cord pia mater in vertebrates].
Fluorimetric studies have been made on the content of adrenalin, noradrenaline, serotonin, dopamine, and tryptamine in the pial matter of the brain and spinal cord of fishes, birds and mammals including man. Using histochemical method with glyoxylic acid, biogenic monoamines were revealed in the adrenergic nerve fibers and monoaminocytes. Their total content in the pial matter of the brain is approximately the same in all vertebrates, being significantly lower in man. Higher concentration of adrenergic axons and lower amount of monoaminocytes in human subjects reveal the key role of the nervous influences in regulation of hemodynamics of the brain.
Adult↗
Identification and quantitative measurements of biogenic monoamines in the central nervous tissue of some gastropods.
Investigations were carried out to determine levels of biogenic monoamines in the central nervous tissue of seven species of terrestrial gastropods (taxonomic family: Helicidae) using high-performance liquid chromatography (HPLC) with electrochemical detection (ELCD). The central nervous tissue of all species examined contained assayable amounts of dopamine (DA) and serotonin (5-HT). Noradrenaline (NA) was occasionally present; adrenaline (A) could not be detected. The central ganglia of two Mediterranean species generally contain 3-4 times more 5-HT relative to DA than the ganglia of the other species which contain amounts of 5-HT only slightly higher than DA.
Animals↗
[Effects of Chinese ginseng root and stem-leaf saponins on learning, memory and biogenic monoamines of brain in rats].
The present investigation has shown that Ginseng root saponins (ig, 50mg/kg x 7d) facilitate the learning and memory of normal male Wistar rats, while the effect of Ginseng stem-leaf saponins (ig, 50mg/kg x 7d) on antielectrconvulsive shock-induced impairment of memory consolidation in rats is more intensive than that of root saponins. Both Ginseng root and stem-leaf saponins can significantly raise the levels of biogenic monoamines in normal rat's brain.
Animals↗
Effect of T-2 toxin on brain biogenic monoamines in rats and chickens.
Two experiments were conducted to determine the effect of T-2 toxin on brain biogenic monoamines and their metabolites. Male rats (180 g) and cockerels (28 day, 300 g) were orally dosed with T-2 toxin at 2.5 mg kg-1 body weight. In the first experiment, whole brains were collected 2, 6, 12, 24 and 48 h postdosing and analyzed for monoamines by high performance liquid chromatography with electro-chemical detection. T-2 toxin did not influence whole brain concentrations of monoamines in either species. In the second experiment, brains were collected 24 h postdosing, dissected into five brain regions, and analyzed for monoamines. T-2 toxin treatment resulted in increased serotonin and 5-hydroxy-3-indoleacetic acid in all brain regions of the rat. However, this was not seen in poultry where T-2 toxin treatment resulted in an increase in 5-hydroxy-3-indoleacetic acid, no alteration in serotonin concentration and a decrease in regional norepinephrine and dopamine concentrations. These results suggest that T-2 toxin influences brain biogenic amine metabolism and that there is an intraspecies difference in the central effects of this mycotoxin.
3,4-Dihydroxyphenylacetic Acid↗
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↗
[The effect of biogenic monoamine antagonists on the development of preimplantation mouse embryos cultured in vitro].
The effect of serotonin and adrenaline antagonists was tested on the early embryos of mice of three lines. All the substances tested produced an arrest or inhibition of cleavage division and the appearance of anomalies. Serotonin introduced in the incubation medium was effective against some serotoninolytics. We were unable to test the protective effect of adrenaline, as in the concentrations used it has its own effect on the development. From the data obtained, a conclusion is made of the existence in early mouse embryos of the structures sensitive to serotonin and adrenaline antagonists. The assumptions is made from the previously obtained data on the presence of biogenic monoamines in early mouse embryos, of functional activity of prospective mediators of the nervous system at the earliest stages of embryonic development of mammals.
Alprenolol↗
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↗