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At least 1,171 records · Page 65Linked to original sources
PubMed1975

d-Amphetamine as a releaser or reuptake inhibitor of biogenic amines in synaptosomes.

The effect of d-amphetamine on the release of tritiated norepinephrine (NE), dopamine (DA) and 5-hydroxytryptamine (5-HT) was analyzed in synaptosomes from different brain area. 3H-NE release was unaffected in the hypothalamus, a region which is rich in noradrenergic terminals, and in cerebellum and pons-medulla, but was substantially increased in corpus striatum and moderately in cerebral cortex. 3H-DA release was strongly enhanced in corpus striatum, a region rich in dopaminergic terminals, substantially increased in cerebral cortex, and slightly increased in the hypothalamus. Since the regional pattern of d-amphetamine-stimulated release was similar with the two catecholamines, but the stimulation was greater with 3H-DA than with 3H-NE, and was more evident in areas richer in dopaminergic terminals, it is suggested that the drug can release 3H-DA or artificially stored 3H-NE from dopaminergic terminals, but not 3H-NE, from noradrenergic terminals. d-Amphetamine also seems capable of releasing 3H-5-HT from serotoninergic terminals. In contrast with the two catecholamines, 3H-5-HT release was more enhanced in cerebral cortex than in corpus striatum.

Animals↗
PubMed1976

Effect of biogenic amines and GABA on ATPase activities in mouse tissue.

ATPase activities were studied in brain, kidney and liver (13,000 X g pellet) fraction from the mouse. Dopamine and norepinephrine added in vitro showed a dose-dependent stimulation of Na+ and K+ activated and oligomycin sensitive Mg2+ ATPase activities in brain but not kidney and liver tissue fractions. GABA and serotonin had no effect on ATPase in brain, but inhibited oligomycin sensitive Mg2+ ATPase activities in kidney and liver. The relationship between the enhancement of ATPase activity by neurotransmitters in brain and the neuronal excitation is discussed.

Adenosine Triphosphatases↗
PubMed1976

Effects of salsolinol on smooth muscle responses to various biogenic amines.

Isolated smooth muscle tissues from rats, guinea pigs and rabbits were used to investigate pharmacological effects of salsolinol (1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline). By itself, salsolinol did not produce any profound or sustained sympathomimetic or 5-hydroxytryptamine-like activity in the concentrations used in these experiments (7.7 and 77 muM). Salsolinol was found to antagonize the contraction of the rabbit aorta induced by noradrenaline but did not affect the adrenaline-induced relaxation of the guinea pig tracheal chain. On both the rat fundus and oestrus rat uterus, salsolinol exhibited significant anti-5-hydroxytryptamine activity but responses of these tissues to acetylcholine and histamine remained unaffected, indicating that the action was not non-specific. These results suggest that in vivo formation of salsolinol after ethanol ingestion could produce significant pharmacological effects.

Acetylcholine↗
PubMed1977

Effects of amphetamine on brain biogenic amines in isolated and aggregated rats.

d- and 1-amphetamine were injected (15 mg/kg i.p.) into isolated or aggregated rats. Both d- and 1-forms decreased the noradrenaline levels of brain areas in isolated and in aggregated rats. d-Amphetamine decreased 5-hydroxytryptamine (5-HT) and 5-hydroxyindolacetic acid (5-hiaa) levels in aggregated rats only. 1-Amphetamine induced no change in 5-HT and 5-HIAA levels. The greater sensitivity of aggregated rats to d-amphetamine can be ascribed to a change in 5-HT metabolism rather than to a modification of noradrenaline levels.

Amphetamine↗
PubMed1978

Effects of viloxazine, its optical isomers and its major metabolites on biogenic amine uptake mechanisms in vitro and in vivo.

Viloxazine hydrochloride (ICI 58,834, VIVALAN) a chemically novel antidepressant, shows selective inhibition of noradrenaline uptake into mouse heart in vivo and into rat brain in vitro. The noradrenaline uptake inhibitory activity resides primarily in one of the two optically active isomers, and it is suggested that in the conformation adopted for uptake by noradrenaline, the aryl and the amino groups are trans. In a comparison of in vivo and in vitro potency, tri- and tetracyclic antidepressants exhibit a good correlation. However, viloxazine possesses higher in vivo activity than would be expected from in vitro studies. The latter finding cannot be readily explained on the basis of known pharmacokinetic or metabolic factors.

Animals↗
PubMed1979

Pretreatment with delta 1-tetrahydrocannabinol and psychoactive drugs: effects on uptake of biogenic amines and on behavior.

Injection of delta 1-tetrahydrocannabinol (THC) into mice increased the uptake into brain synaptosomes of radioactive DA, NE, 5-HT and GABA, with the effect on GABA being the greatest; uptake of leucine was not stimulated, indicating that THC does not facilitate the transport of amino acids in general. The effect of THC was stereospecific because pretreatment with the non-psychoactive isomer, (+) delta 6-THC had no effect on uptake of DA into cortical synaptosomes. The effect on DA uptake was correlated with psychoactive potency. THC enhanced uptake more than did SP-111 (a water soluble ester of THC but less potent than THC) and much more than cannabidiol (a non-psychoactive ingredient of marijuana). THC increased the uptake of DA into striatal synaptosomes but much less than into cortical synaptosomes. The enhancing effect of THC on uptake in cortex showed tolerance after chronic (1 week) treatment with THC. Catecholaminergic receptor antagonists (chlorpromazine, propranolol), like THC, stimulated the uptake of DA or NE into cortical synaptosomer. In contrast, pretreatment with MAO (pargyline) or uptake (tricyclic antidepressants) inhibitors, or with amphetamine, decreased uptake. Thus THC does not inhibit MAO uptake, or stimulate the release of catecholamines but may interact with a receptor. The notion of a THC--receptor interaction is supported by behavioral experiments.

Animals↗
PubMed1982

Different effects of behaviorally equipotent doses of amphetamine and methamphetamine on brain biogenic amines: specific increase of phenylethylamine by amphetamine.

The effects of acute semichronic (twice daily for three days) treatments with the same doses of amphetamine (AMPH) and methamphetamine (M-AMPH) on rat brain phenylethylamine (PEA) and catecholamines were evaluated. These treatments produced similar behavioral responses and hence are assumed to be generally equipotent. Both drugs entered the brain rapidly but at different rates. While AMPH and M-AMPH produced comparable changes in the contents of catecholamines and their metabolites in the hypothalamus and caudate nucleus, only AMPH significantly elevated PEA. The elevated brain PEA produced by AMPH was not due to alpha-demethylation of AMPH. It is concluded that brain PEA may mediate some of AMPH behavioral effects but not those of M-AMPH. The catecholamines appear to be involved in the effects of both drugs.

Amphetamine↗
PubMed1986

The effects of desipramine, zimelidine, electroconvulsive treatment and lithium on rat brain biogenic amines: a comparison with peripheral changes.

The effects of 4 common treatments for affective disorders on total body norepinephrine (NE) and dopamine (DA) turnover and metabolism were evaluated in rats. The treatments were chronic desipramine (DMI), zimelidine (ZMI), electroconvulsion (ECT) and lithium (Li). The central effects of ECT and Li were also assessed in the brain. The results obtained were compared with the effects of these 4 treatments on total NE (Sum NE) and DA (Sum DA) turnover in depressed patients. We have also evaluated central and/or peripheral effects of these treatments on phenylethylamine, p-tyramine and serotonin metabolism. The urinary changes in Sum NE and DA observed after DMI, ZMI and Li in the rat were similar to those found in depressed patients; Sum NE was significantly reduced. In contrast to its effects on depressed patients, chronic ECT significantly increased Sum NE. Similar to depressed patients, ECT reduced the fraction of NE escaping re-uptake in the rat. Sum DA was not affected by DMI, ZMI or ECT, but was significantly reduced by chronic Li treatment. All 4 treatments significantly reduced serotonin metabolism as indicated by reduced 5-hydroxyindoleacetic acid excretion rates. DMI, ZMI and Li treatments significantly reduced phenylethylamine urinary but not p-tyramine urinary outputs. The opposite effect was observed after ECT. Consistent with their effects on Sum NE, Li reduced while ECT increased hypothalamic NE turnover as deduced from the changes in 3-methoxy-4-hydroxyphenylglycol's rate of formation. As for Sum DA, Li had no effect on 3,4-dihydroxyphenylacetic acid or homovanillic acid's rates of formation in the caudate nucleus. Chronic ECT produced a small, but significant increase in homovanillic acid's rate of formation in the caudate nucleus.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1988

Chronic cocaine effects on peripheral biogenic amines: a long-term reduction in peripheral dopamine and phenylethylamine production.

The short- (during 12 h after last treatment) and long- (6 weeks after last treatment) term effects of repeated administration of cocaine on the total output of norepinephrine (NE) and its metabolites (sum NE), dopamine (DA) and its metabolites (sum DA) as well as the excretion of 5-hydroxyindoleacetic acid (5-HIAA) and phenylethylamine were evaluated in rats. The concentration of NE, DA and 3,4-dihydroxyphenylacetic acid (DOPAC) in the celiac ganglion after 1, 2 and 3 weeks of repeated cocaine administration were also measured. Sum NE remained unchanged during the cocaine treatment but NE and normetanephrine excretions were significantly decreased and increased respectively. 5-HIAA excretion was significantly reduced only after 3 weeks cocaine treatment. In the celiac ganglion NE and DOPAC contents showed tendencies towards being increased and decreased respectively. DA content was not changed. The excretions of DA, DOPAC, homovanillic acid (HVA) and phenylethylamine were significantly reduced during chronic exposure to cocaine. The above short-term changes in DA and phenylethylamine persisted for periods as long as 6 weeks after 1 week repeated exposure to cocaine. It is concluded that chronic exposure to cocaine can produce preferential long term deficiencies in the production of DA and phenylethylamine in the periphery. Peripheral noradrenergic and serotonergic neuronal systems are apparently minimally affected. The close association between DA or sum DA and phenylethylamine excretion suggest these 2 amines may coexist in the same neuron.

3,4-Dihydroxyphenylacetic Acid↗