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PubMed1977

Some effects of mazindol, an anorectic drug, on rat brain monoaminergic systems.

Mazindol was devoid of effect both on rat brain steady state levels of 5-HT, 5-HIAA and tryptophan and on the rate of synthesis of 5-HT in the rat brain. Mazindol had no effect on rat brain 5-HT uptake in vivo as determined by the effect of drug pretreatment on the ability of p-chloroamphetamine to lower central 5-HT levels. A large dose of mazindol caused a slight transient decrease in rat brain levels of NA and DA. Blockade of rat brain catecholamine uptake was quantified by studying drug effects on the ability of intraventricularly administered 6-hydroxydopamine to lower brain NA and DA content. Mazindol was an extremely potent inhibitor of rat brain NA uptake in vivo, being 4-5 times more potent than desipramine. Mazindol also blocked rat brain DA uptake. Doses of mazindol needed to release alpha-methyl-m-tyramine from the rat striatum were appreciably greater than the corresponding doses of d-amphetamine. The neurochemical profile of mazindol bears a much closer resemblance to that of d-amphetamine than to that of fenfluramine.

Animals↗
PubMed1978

Distribution and localization of p-hydroxy-d-amphetamine in rat brain.

p-Hydroxy-d-amphetamine (p-OHdA) penetrates the blood--brain barrier poorly, when given acutely or by repeated systemic treatments, or when formed by biotransformation from administered d-amphetamine. However its distribution is relatively selective as it accumulates in the striatum more than in the brainstem. The rate of disappearance also differs in the two areas, being slower in the striatum than in the brainstem. These findings suggest that p-OHdA might be stored in different compartments. To check whether p-OHdA specificially accumulated in nerve terminals, catecholaminergic nerve endings were destroyed with 6-hydroxydopamine (6-OHDA). It has been shown that p-HOdA accumulates much less in the striatum of 6-OHDA-treated rats than of controls. This effect was not present in the brainstem. Accumulation of p-OHdA was similar after repeated d-amphetamine administration. The results are interpreted as showing that p-OHdA tends to accumulate in dopaminergic structures.

Amphetamines↗
PubMed1979

Interindividual and interspecies variation in the metabolism of the hallucinogen 4-methoxyamphetamine.

1. The qualitative and quantitative aspects of the urinary elimination of orally administered 4-methoxy[14C]amphetamine have been examined in the rat and guinea-pig and in three volunteer human subjects, to determine interspecies and interindividual variations in disposition of the drug. 2. Both rat and guinea-pig excreted 70--80% of the administered dose(6 mg/kg) in the urine within 24 h, mainly as metabolites. 3. In the guinea-pig, the drug was metabolized by O-demethylation to give 4-hydroxyamphetamine, which was excreted free (4% dose) and conjugated (73%). No other metabolite was detected. 4. The rat metabolizes the drug both by O-dealkylation and by side-chain oxidation, the products being 4-hydroxyamphetamine (5% of dose free and 60% conjugated) and 1-(4'-methoxyphenyl)propan-2-one oxime (5% dose, free and conjugated). 5. In man the drug (dose 5 mg) is metabolized by O-demethylation and by side-chain oxidation. Marked intersubject variations were observed both in the array and quantitative aspects of metabolite excretion. Two subjects excreted mainly 4-hydroxyamphetamine (free and conjugated) together with smaller amounts of 1-(4'-methoxyphenyl)propan-2-one oxime and 4-hydroxynorephedrine. The third subject, however, who was previously known to exhibit a genetically determined defect in drug oxidation, was defective in O-dealkylation of 4-methoxyamphetamine, and the main excretion products were the unchanged drug together with products of side-chain oxidation, namely, 1-(4'-methoxyphenyl)propan-2-one oxime, 1-(4'-methoxyphenyl)propan-2-one and 4-methoxybenzoic acid. 6. Inter-individual differences in oxidative O-demethylation of the drug are discussed in relation to current theories on the aetiology of schizophrenia and reported fatalities arising from abuse of the drug.

Adult↗
PubMed1976

Thin layer chromatographic identification of some sympathomimetic amines.

Thin layer chromatographic behavior of some sympathomimetic amines in the presence of acids in neutral and organic solvent systems is reported. The sympathomimetic amines were dissolved in 0.1N HCl or ethanol and treated with bromocresol green or p-nitrobenzoyl chloride reagents on fiber sheets or precoated glass plates. Two-, 3-, and 4-, component solvent systems were tested. Benzene-ethyl acetate gave 2 spots for each amine standard; the more polar spots were satisfactorily separated. Amines in pharmaccuticals were not separated by any solvent system tested.

Amines↗
PubMed1976

Discriminative response control by psychomotor stimulants.

Psychomotor stimulants are capable of controlling discriminative responding in rats. Evidence suggests that response control is central, of a fairly specific nature, and dependent on intact dopaminergic functions.

DOM 2,5-Dimethoxy-4-Methylamphetamine↗
PubMed1975

Studies on the mechanism of depletion of striatal dopamine by alpha-methyl-m-tyrosine.

These experiments were designed to study the mechanism of depletion of dopamine (DA) in the striatum produced by alpha-methyl-m-tyrosine (alpha-MMT). alpha-Methyl-m-tyramine (alpha-MMTA), the metabolite of alpha-MMT, appears to be the active DA-depleting agent, since the administration of a decarboxylase inhibitor before alpha-MMT markedly reduced both the formation of alpha-MMTA and the depletion of DA. After injection of alpha-MMT (100 mg/kg i.p.), the striatal concentration of homovanillic acid (HVA) rose by 41% at 1 hour. This is probably due to an increase in DA metabolism, since alpha-MMT markedly enhanced the decline of DA produced by alpha-methyl-p-tyrosine (alpha-MPT). At 2, 3 and 4 hours after alpha-MMT, the concentration of HVA and dihydroxyphenylacetic acid was below control level. The decrease in dihydroxyphenylacetic acid is due partially to a decreased formation of dihydroxyphenylacetic acid from DA. In striatal slices, both alpha-MMT and alpha-MMTA decreased the formation of 3H-H2O and the accumulation of 3H-DA from 1-3,5-3H-tyrosine. Alpha-MMT did not alter the specific activity of 3H-tyrosine or release 3H-DA from the slices, but it did inhibit the activity of tyrosine hydroxylase in striatal homogenates at low concentrations of tyrosine (10 muM). Alpha-MMTA released both newly synthesized and exogenously accumulated 3H-DA from striatal slices. At low concentrations of alpha-MMTA, the percent reduction in 3H-H2O was much greater than the percentage of 3H-DA released into the medium. However, at higher concentrations, the inhibition of 3H-H2O reached a maximum while 3H-DA release kept increasing. These results suggest that both inhibition of tyrosine hydroxylase activity and DA release from storage sites by alpha-MMTA may account for the depletion of DA produced by the injection of alpha-MMT.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1975

[Comparative subcellular localization of para-hydroxylated derivatives of ephedrine and amphetamine in rat brain].

Localisation of noradrenaline, hydroxyamphetamine, hydroxynorephedrine and hydroxyephedrine was studied in adrenergic granules of rat's brain in normal animals and in animals injected with hydroxy-6 dopamine. In normal animals the synaptosomes fixed noradrenaline, first and then, in decreasing order, hydroxynorephedrine, hydroxyephedrine and hydroxyamphetamine. Hydroxy-6 dopamine injection resulted in a decrease of fixation by synaptosomes, thus confirming the role of central false-transmitters of hydroxylated derivatives of amphetamine and ephedrine.

Amphetamines↗
PubMed1977

Sympathetic pupillary activity in infants.

In an attempt to learn the contribution of the sympathetic system to smaller pupillary size in infants, pupillary responses were tested to agents acting on this system in 12 ihfants and 23 young adults. Phenylephrine dilated the pupils of both groups by the same ratio, with infants' pupils reaching a lesser diameter. The responses to cocaine and hydroxyamphetamine were lower in children. It is concluded that in the first months of life the postganglionic sympathetic nerve releases less norepinephrine. This may be due to a lower number of sympathetic neurons. The post-synaptic apparatus may not be fully developed in infants.

Adolescent↗