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At least 1,063 records · Page 59Linked to original sources
PubMed1976

Head twitches induced by benzodiazepines and the role of biogenic amines.

Clonazepam, one of the benzodiazepines, induced head twitches in mice in a dose-dependent manner and sustained them for at least 120 min. Some of the benzodiazepines such as nitrazepam, fludiazepam, and nimetazepam also significantly induced head twitches at doses higher than 10 mg/kg, but other benzodiazepines like diazepam, flurazepam, oxazepam, medazepam, and chlordiazepoxide did not significantly induce head twitches at doses up to 60 mg/kg. The head twitches induced by clonazepam were more strongly blocked by a n antiserotonin drug, cyproheptadine than catecholamine receptor blocking drugs, haloperidol, propranolol, and phentolamine, and were not blocked by GABA receptor blocking drugs, bicuculline and picrotoxin, as well as by a glycine receptor blocking drug, strychnine. Clonazepam also increased the head twitches induced by mescaline, a serotonin receptor stimulant. These results indicate that the head twitches induced by clonazepam might be mediated via serotonergic neuron systems.

Animals↗
PubMed1975

Involvement of biogenic amines in drug-induced aggressive pecking in chicks.

Pairs of neonate chicks were administered psychoactive agents and pecks against each other were recorded during 4-hr test sessions. The first experiment assessed where drug-induced aggressive pecking could serve as a useful anti-depressant screening model. Although pecking was induced by tricyclics, d-amphetamine, and L-Dopa, ineffective agents included a MAO inhibitor (pargline) and a tricyclic indole antidepressant (iprindole). These data cast doubt on the validity of the chick pecking model as a specific antidepressant tests. A second experiment attempted to determine where different amines were involved in pecking induced by an antidepressant and a CNS stimulant. Pairs of chicks were pretreated with various doses of amine antagonists, and a standard dose of imipramine (IMI) or d-amphetamine (AMP) was administered. Haloperidol completely antagonized AMP but not IMI pecking, while phentolamine and propranolol did not modify AMP pecking, suggesting involvement of dopamine. Pecking induced by IMI was partially antagonized by a dose of methysergide ineffective in modifying AMP pecking. Neither phentolamine nor propranolol blocked IMI pecking. Serotonin was further implicated in IMI pecking in a third experiment, whether chronic PCPA pretreatment significantly decreased IMI, but not AMP pecking. These data suggest that aggressive pecking induced by AMP and IMI may be mediated by different amine systems.

Aggression↗
PubMed1976

Effects of pyrroxan and chlordiazepoxide on biogenic amine metabolism in the rat brain.

Pyrroxan (20 mg/kg, i.p.), a new potential antianxiety agent, increased brain norepinephrine (NE) turnover in rats, reflecting a possible central alpha-adrenergic receptor blocking activity. In contrast, chlordiazepoxide (20 mg/kg, i.p.), a widely used antianxiety agent, did not alter the NE turnover. Pyrroxan did not affect overall DA turnover although it did appear to accelerate DA turnover initially. The initial potentiation of DA turnover may indicate a short-lasting blocking action on DA receptors. In comparison, chlordiazepoxide (20 mg/kg, i.p.) decreased the turnover rate of DA. Effects of both drugs on 5-HT indicate a decrease in turnover with no significant monoamine oxidase activity or blockade of the 5-HT reuptake mechanism. Both drugs antagonized the decline in intraventicularly-injected 14C-5-HT. Neither drug caused consistent changes in endogenous 5-HT, 5-hydroxyindoleacetic acid, or tryptophan levels. Neither drug potentiated the behavioral effects of L-Dopa nor increased the 5-HTP behavoiral syndrome in the mouse. Pyrroxan may be expected to exhibit a spectrum of activity between that of minor and major tranquilizers, characterized by antianxiety action together with sedative or tranquilizing activity.

Animals↗
PubMed1984

Platelets and biogenic amines. 1. Platelets are poor investigative models for dopamine re-uptake.

The uptake of 14C-dopamine (DA) by human platelets at 10(-7) -2.5 X 10(-4) M of labelled amine concentration was studied in human platelet-rich plasma. The total uptake could be resolved into two components, one of which was saturable and completely inhibited by 10(-5) imipramine and another which was unsaturable but temperature-dependent. The saturable uptake of DA had an apparent Km of 75 X 10(-6) M and Vmax of 1.34 pmol/10(6) platelets/min. The uptake of unsaturable DA was 1.33 pmol/10(6) platelets/min at 10(-4) M DA. Dopamine exerted a mixed non-competitive inhibition of the saturable 5-HT transport and vice versa. Thus the increase in Km was paralleled by a decrease in Vmax. The low-affinity transport of DA by the human platelets does not share any of the dopamine uptake characteristics found in neuronal tissue. The platelet therefore seems to be a poor model for the presynaptic function of the dopamine neurons.

Biogenic Amines↗
PubMed1981

Effects of acute administration of cyclazocine on the metabolism of biogenic amines in different regions of rat brain.

The effects of cyclazocine on the metabolism of dopamine (DA), noradrenaline (NA) and 5-hydroxytryptamine (5-HT) in regions of rat brain were studied by measuring changes in the levels of the monoamines and their major metabolites. Doses ranging from 4-32 mg/kg were tested. Rats were sacrificed 1 or 2 h after administration of the drug, according to the experiment. Administration of cyclazocine significantly decreased DA concentration and increased the levels of DOPAC and HVA in striatum. Cyclazocine decreased the levels of NA, and markedly increased the levels of MHPG-SP4 and 5-HIAA in cortex, hypothalamus, midbrain and pons-medulla, while little change in 5-HT concentration, except a decrease after the highest dose, was observed. These changes in the metabolism of the monoamines differed in their amplitude and temporal nature. The possible roles of dopaminergic, noradrenergic and serotoninergic neurons in different brain regions are discussed in relation to modifications of locomotor activity and the induction of bizarre behavior resulting from cyclazocine administration in rats. These investigations may add to the understanding of the mechanism of psychotomimetic effects produced in man by this drug.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1977

Uptake inhibition of biogenic amines by newer antidepressant drugs: relevance to the dopamine hypothesis of depression.

The dopamine theory of depression was studied by assessing the effect of antidepressant drugs on uptake of dopamine, noradrenaline, and serotonin in synaptosomes from rat brain. Five newer drugs--butriptyline, maprotiline, trimipramine, iprindole, and mianserine--exhibited rather potent inhibition of 3H-dopamine uptake in corpus striatum, as their IC50 values, which were in the order of 10(-6)-10(-5) M, were only about 50 times higher than for nomifensine (IC50 = 10(-7) M). The five drugs were weak, compared to chlorimipramine, on 14C-serotonin uptake in the whole forebrain, as their IC50 were about 10(-5) M. Butriptyline, trimipramine, and iprindole were very weak uptake inhibitors of 3H-noradrenaline in the occipital cortex. Their IC50 values were about 10(-6) M, which is almost 1000 times higher than for desmethylimipramine. These results are discussed in relation to comprehensive recent literature as further indicating a link between dopamine and depression.

Animals↗
PubMed1976

Competition of some biogenic amines for uptake into synaptic vesicles of the striatum.

Synaptic vesicles were isolated from the caudate nucleus of the pigs by differential centrifugation and incubated with labelled monoamines in the absence or in the presence of ATP-Mg(2+). Addition of ATP-Mg(2+) enhanced the uptake of (14)C-dopamine into the vesicles. Serotonin competitively inhibited the ATP-Mg(2+)-dependent uptake of (14)C-dopamine without influencing the uptake which took place in the absence of ATP-Mg(2+). Likewise, dopamine caused a dose-dependent inhibition of the ATP-Mg(2+)-dependent uptake of (14)C-serotonin without inhibiting the uptake in the absence of ATP-Mg(2+). Incubation of the vesicles with equal concentrations of(3)-dopamine and (14)C-serotonin revealed that the presence of the one amine competitively inhibited the ATP-Mg(2+)-dependent uptake of the other. Tyranimine competitively inhibited the ATP-Mg(2+)-dependent uptake of (14)C-dine, (14)C-serotonin and (14)C-noradrenaline into the vesicles; the uptake of the amines which took place in the absence of ATP-Mg(2+) was not impairedby tyramine. Analysis of the amine uptake by the ABC test showed that a mutual inhibition exists between dopamine and serotonin for the uptake into the synaptic vesicles. GABA did not influence the uptake of (14)C-dopamine either in the absence, or in the presence of ATP-Mg(2+)...

Adenosine Triphosphate↗
PubMed1986

Binding of psychoactive drugs to rat brain amine receptors, measured ex vivo, and their effects on the metabolism of biogenic amines.

Ex vivo receptor binding experiments and measurements of the concentrations of the amine metabolites HVA, MOPEG-SO4 and 5-HIAA were carried out on rat brain tissues to analyse the effects of several neuroleptics (haloperidol, chlorpromazine, thioridazine, clozapine, fluperlapine), antidepressants (amitriptyline, mianserin, zimelidine) and other drugs (pizotifen, ketanserin, prazosin) on brain aminergic systems. It was found that in all cases where drugs reduced 3H-haloperidol binding to striatal D2-receptors ex vivo (haloperidol, chlorpromazine, thioridazine, clozapine, fluperlapine, pizotifen, zimelidine), the same drugs caused a pronounced increase, in vivo, in the striatal HVA-concentration, i.e. an increase in DA-turnover. The HVA-increase was directly proportional to the extent of the reduction of 3H-haloperidol binding. These findings suggested that in the 3H-haloperidol assay binding of drugs is to functional D2-receptors regulating the release of DA. In contrast, reduction of binding of 3H-prazosin to brain stem alpha 1-receptors ex vivo (all drugs except zimelidine) was only associated with an in vivo increase in the MOPEG-SO4 concentration in some cases (haloperidol, chlorpromazine, thioridazine, clozapine, fluperlapine, ketanserine). Similarly, reduction of 3H-spiperone binding to 5-HT2-receptors in the frontal cortex (all agents except prazosin and zimelidine) was only associated with an increase in the 5-HIAA concentration in certain cases (thioridazine, clozapine, fluperlapine, pizotifen, ketanserin). The present data indicate that in the brain alpha 1- and 5-HT2-receptors do not seem to be linked directly to the processes which govern the turnover of the neurotransmitters DA, NA or 5-HT.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1976

A comparison of the central actions of prostaglandins A1, E1, E2, F1alpha, and F2alpha in the rat. II. The effect of intraventricular prostaglandins on the action of some drugs and on the level and turnover of biogenic amines in the rat brain.

Prostaglandins (PGs) injected into the right lateral brain ventricle (i.v.c.) of the rat increased the sleeping time induced by hexobarbital, chloral hydrate, and ethanol. PGE1 and PGE2 intensified chlorpromazine-induced catalepsy, inhibited amphetamine hyperactivity, and significantly depressed the amphetamine-induced stereotypy. NA concentrations were decreased by PGE1 and PGE2 and were increased by PGF2alpha. PGF2alpha increased both 5-HT and 5-HIAA levels in rat brain. "Total" ACh concentrations were increased by PGF1alpha and PGF2alpha. PGE1, PGE2, and PGF2alpha enhanced the turnover of NA, DA, and 5-HT. PGE2 counteracted the decreased activity induced by alpha-MT and abolished the hypothermic action of alpha-MT. PGF2alpha had little effect on the activity of PCPA pretreated rats, whereas the higher doses of PGF2alpha increased body temperature in these animals.

Acetylcholine↗
PubMed1983

Effects of CGP 11305 A, a new reversible and selective inhibitor of MAO A, on biogenic amine levels and metabolism in the rat brain.

CGP 11305 A [4-(5-methoxy-7-bromo-benzofuranyl-2)piperidine HCl), a reversible, selective inhibitor of MAO A, increased the levels of rat brain noradrenaline, dopamine, and serotonin dose-dependently and to approximately the same extent. Concomitantly, it lowered the levels of their metabolites, MHPG-SO4, HVA, DOPAC, and 5-HIAA. When compared with the irreversible MAO A inhibitor clorgyline, the effects of CGP 11305 A were of much shorter duration. Moreover, the increases of noradrenaline and serotonin and the decreases of their metabolites MHPG-SO4 and 5-HIAA were smaller after CGP 11305 A than after clorgyline in equieffective doses for MAO A inhibition. CGP 11305 A decreased the synthesis of catecholamines and serotonin less markedly than clorgyline. This is probably due to the reversibility of the interaction of the compound with MAO A. In contrast to CGP 11305 A, clorgyline increased the level of dopamine less than those of noradrenaline and serotonin. This is explained by assuming that dopamine synthesis is particularly sensitive to end product inhibition. CGP 11305 A also exhibited some inhibitory properties on the uptake of serotonin and, to a lesser degree, of noradrenaline in vitro and in vivo. Compared with MAO inhibition, however, uptake inhibition required 30-100 times higher doses.

Animals↗
PubMed1992

Effects of whole body microwave exposure on the rat brain contents of biogenic amines.

The effects of whole body microwave exposure on the central nervous system (CNS) of the rat were investigated. Rats weighing from 250 to 320 g were exposed for 1 h to whole body microwave with a frequency of 2450 MHz at power densities of 5 and 10 mW.cm-2 at an ambient temperature of 21-23 degrees C. The rectal temperatures of the rats were measured just before and after microwave exposure and mono-amines and their metabolites in various discrete brain regions were determined after microwave exposure. Microwave exposure at power densities of 5 and 10 mW.cm-2 increased the mean rectal temperature by 2.3 degrees C and 3.4 degrees C, respectively. The noradrenaline content in the hypothalamus was significantly reduced after microwave exposure at a power density of 10 mW.cm-2. There were no differences in the dopamine (DA) content of any region of the brain between microwave exposed rats and control rats. The dihydroxyphenyl acetic acid (DOPAC) content, the main metabolite of DA, was significantly increased in the pons plus medulla oblongata only at a power density of 10 mW.cm-2. The DA turnover rates, the DOPAC:DA ratio, in the striatum and cerebral cortex were significantly increased only at a power density of 10 mW.cm-2. The serotonin (5-hydroxytryptamine, 5-HT) content in all regions of the brain of microwave exposed rats was not different from that of the control rats. The 5-hydroxyindoleacetic acid (5-HIAA) content in the cerebral cortex of microwave exposed rats was significantly increased at power densities of 5 and 10 mW.cm-2.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗