Biomedical subjects
J Axelrod
Publications and source records attributed to J Axelrod.
Brain tryptamine and the effects of drugs.
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Genetically controlled alterations in the rate of degradation of phenylethanolamine N-methyltransferase.
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Elevated plasma dopamine-beta-hydroxylase activity in autosomal dominant torsion dystonia.
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Delta-9-tetrahydrocannabinol: localization in body fat.
[(14)C]Delta(9)-Tetrahydrocannabinol (Delta(9)THC) was injected subcutaneously in rats every day for 1 to 26 days. Concentrations of Delta(9)THC and its metabolites, 11-hydroxytetrahydrocannabinol and 8,11-dihydroxytetrahydrocannabinol, were determined in various tissues. After a single injection, the concentration of Delta(9)THC in fat was ten times greater than in any other tissue examined, and persisted in this tissue for 2 weeks. With repeated injection, Delta(9)THC and its metabolites accumulated in fat and brain.
Dopaminergic neurons in explants of substantia nigra in culture.
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Demonstration and distribution of phenylethanolamine in brain and other tissues.
A specific and sensitive assay for phenylethanolamine in tissues is described. By this assay, phenylethanolamine was detected in many peripheral tissues and brains of rats. It is unequally distributed in rat brain, with the highest concentration present in hypothalamus and midbrain. Concentrations of brain phenylethanolamine were elevated after administration of phenylethylamine, phenylalanine, p-chlorophenylalanine, and monoamine oxidase inhibitors and decreased after administration of dopamine-beta-hydroxylase inhibitors. Denervation of sympathetic nerves caused a moderate fall in phenylethanolamine concentrations. These results indicate that phenylethanolamine is synthesized intraneuronally from phenylalanine and phenylethylamine, but that only part of the phenylethanolamine is stored in sympathetic nerves.
Supersensitivity and subsensitivity of the beta-adrenergic receptor in pineal gland regulated by catecholamine transmitter.
Depletion of neural norepinephrine by reserpine treatment or by denervation resulted in a greater induction of serotonin N-acetyltransferase (EC 2.3.1.5) and a higher elevation of cyclic AMP in postsynaptic pineal cell to small amount of isoproterenol. This increase in responsiveness occurs rapidly within 24 hr after treatment with reserpine. Repeated administration of isoproterenol to the denervated or reserpine-treated rats not only suppressed the superinduction, but also caused a decreased response to isoproterenol in cultured pineal cells. Cultured pineal cells from denervated or reserpine-treated rats were about 10 times more responsive to small amounts of isoproterenol. The response of cultured pineal cells of rats which were repeatedly injected with isoproterenol was markedly reduced after exposure to submaximal amounts of catecholamines. The maximal increase in N-acetyltransferase was the same in denervated, reserpine-treated, isoproterenol-treated, and untreated pineal cells. Exposure of rats to continuous lighting (a procedure that reduces sympathetic nerve activity) resulted in a superinduction of pineal N-acetyltransferase by isoproterenol. These observations indicate that the responsiveness of the postsynaptic beta-adrenergic receptor is conditioned by prior exposure to its agonist, norepinephrine. Decreased norepinephrine results in supersensitivity, and repeated exposure to large amounts of catecholamines causes subsensitivity (tolerance).
The distribution and properties of the nonspecific N-methyltransferase in brain.
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Effect of dexamethasone on phenylethanolamine N-methyltransferase in chromaffin tissue of the neonatal rat.
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A dimethyltryptamine-forming enzyme in human blood.
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Endocarditis caused by Lactobacillus plantarum.
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The fate of noradrenaline in the sympathetic neurone.
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The regulation of pineal serotonin by a beta adrenergic receptor.
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Control of pineal N-acetylserotonin by a beta adrenergic receptor.
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Effect of drugs on the tryptamine content of rat tissues.
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Nobel Prize winner talks about noradrenaline, nerves and aging.
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Enhanced release of dopamine -hydroxylase and norepinephrine from sympathetic nerves by dibutyryl cyclic adenosine 3', 5'-monophosphate and theophylline.
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