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PubMed1982

Differential effects of fluoxetine and zimelidine on the uptake of 5-hydroxytryptamine and tryptamine by cortical slices and on responses of cortical neurones to stimulation of the nucleus raphe medianus.

Intravenous administration of fluoxetine inhibited the uptake of tryptamine and 5-hydroxytryptamine by cortical slices. In contrast, zimelidine inhibited the uptake of 4-hydroxytryptamine only. In vivo, inhibitory and excitatory response of cortical neurones to stimulation of raphe medianus were potentiated by fluoxetine whereas only excitatory responses were enhanced by zimelidine. The results are consistent with the suggestion that the inhibitory effects of raphe stimulation are mediated by tryptamine and the excitatory responses by 5-hydroxytryptamine.

Animals↗
PubMed1984

Kynuramine: high affinity for [3H]tryptamine binding sites.

Kynuramine, an endogenously occurring metabolite of L-tryptophan, was found to displace [3H]tryptamine from its high affinity binding sites in rat brain cortex with an inhibition constant (Ki) of 28 nM. Kynuramine exhibited structural specificity and considerable selectivity, compared with its affinity for serotonergic, adrenergic and benzodiazepine recognition sites. This novel finding opens-up the possibility that kynuramine may exert physiological actions via the putative tryptamine receptor.

Animals↗
PubMed1984

High affinity (3H)tryptamine binding sites in various organs of the rat.

(3H)Tryptamine binds with high affinity (KD values around 4 nmol/l) to membranes from different organs of the rat. The number of binding sites was high in the liver, intermediate in the heart and cerebral cortex and low in other organs including ileum, kidney, spleen, stomach and lung. Binding to kidney membranes was investigated in more detail. It was rapid and reversible (t1/2 7 min.). The structure-activity profile was characterized by high affinity of some beta-carbolines (IC50 = 20 - 200 nmol/l), medium affinity of serotonin (IC50 = 858 nmol/l) and low of methysergide (IC50 greater than 20 mumol/l). The findings correlate very well with binding characteristics to cerebral cortex membranes. Therefore, rat brain cortex and other organs contain the same type of (3H)tryptamine binding site and may be equally appropriate for further analysis.

Animals↗
PubMed1992

Neurochemical changes in the rat brain after intraventricular administration of tryptamine-4,5-dione.

Tryptamine-4,5-dione (4,5-DKT) a neurotoxic derivative of serotonin (5-HT), was injected into the lateral ventricle of the rat in order to evaluate its biochemical effects. The levels of 8 substances in the hippocampus, striatum and prefrontal cortex were examined 3, 7 and 14 days after treatment with 4,5-DKT. 5-Hydroxytryptamine and 5-hydroxyindoleacetic acid (5-HIAA) levels were decreased in all three regions by days 7 and 14, respectively. Tryptamine-4,5-dione had no significant effect on dopaminergic or adrenergic systems or on the levels of L-tryptophan and L-tyrosine, in any of the three areas of brain examined. Reduced activity of tryptophan hydroxylase in the cortex was observed 14 days after administration of 4,5-DKT. However, administration of 4,5-DKT did not alter the binding of [3H]paroxetine, a specific antagonist of the uptake of 5-HT, to nerve terminals. These results indicate that 4,5-DKT produced depletion of 5-HT without eliminating serotoninergic nerve terminals.

Animals↗
PubMed2004

Binding of tryptamine analogs at h5-HT1E receptors: a structure-affinity investigation.

Structure-affinity requirements for the binding of serotonin (5-HT) analogs at human 5-HT1E receptors were investigated by examining the affinities of >40 tryptamine-related compounds. No tryptamine analog was found to bind with substantially higher affinity than 5-HT. The results indicate that hydrogen bonding plays a key role in the 5-HT1E/receptor interaction. This finding was supported using quantitative structure-activity analysis (QSAR) techniques such as comparative molecular field analysis (CoMFA) and the program QsarIS.

Cell Line↗
PubMed2004

Tryptamine-based human beta3-adrenergic receptor agonists. Part 2: SAR of the methylene derivatives.

A series of tryptamine derivatives with modified sulfonamide were designed, synthesized, and evaluated for their ability to stimulate cAMP accumulation in CHO cells expressing the cloned human beta3-adrenergic receptor (AR). For this series of compounds, our objective was to symmetrize the alpha-position of the tryptamine moiety maintaining its activity and reducing the cost of production. Compound 11h, having m-aminobenzene, exhibited excellent agonistic activity for beta3-AR with excellent subtype selectivity.

Adrenergic beta-3 Receptor Agonists↗
PubMed2004

Tryptamine-based human beta3-adrenergic receptor agonists. Part 1: SAR studies of the 7-position of the indole ring.

A series of tryptamine-based 2-thiophenesulfonamide derivatives were prepared and their agonistic activity for the beta-adrenergic receptors (ARs) was evaluated. Compound 54, containing 7-methanesulfonyloxy tryptamine, was found to be a highly potent beta3-AR agonist (EC50=0.21 nM, IA=97%) with excellent selectivity for the beta3-AR over the beta1- and beta2-ARs (210- and 86-fold, respectively).

Adrenergic beta-1 Receptor Agonists↗
PubMed2005

Tryptamine and homotryptamine-based sulfonamides as potent and selective inhibitors of 15-lipoxygenase.

A series of inhibitors of mammalian 15-lipoxygenase based on tryptamine and homotryptamine scaffolds is described. Compounds with aryl substituents at C-2 of the indole core of tryptamine and homotryptamine sulfonamides (e.g., 37a-p) proved to be potent inhibitors of the isolated enzyme. Selected compounds also demonstrated desirable inhibition selectivities over isozymes 5- and P-12-LO.

Animals↗
PubMed2004

Pharmacological studies with endogenous enhancer substances: beta-phenylethylamine, tryptamine, and their synthetic derivatives.

The discovery of enhancer regulation in the mesencephalon and the concept that it plays a key role in the operation of innate and acquired drives [Neurochem. Res. 28 (2003) 1187] sets the trace amines (TAs) in their true physiological perspective. The regulation is defined as the existence of enhancer-sensitive neurons in the brain capable of working in a split-second on a high activity level due to endogenous enhancer substances. For the time being, only beta-phenylethylamine (PEA) and tryptamine are the experimentally analyzed examples. (-)-Deprenyl (selegiline), widely used in Parkinson's disease and Alzheimer's disease today, and known as the first selective monoamine oxidase (MAO) type-B inhibitor for decades, was identified as a PEA-derived synthetic mesencephalic enhancer substance. An important and convincing confirmation of the enhancer concept was the recent development of a highly specific and potent tryptamine-derived synthetic mesencephalic enhancer substance, (-)-1-(benzofuran-2-yl)-2-propylaminopentane [(-)-BPAP]. This substance, which is specific and hundreds of times more potent than selegiline, is now the best experimental tool to study the enhancer regulation in the mesencephalon and a promising candidate to significantly surpass the therapeutic efficiency of selegiline in depression, Parkinson's disease, and Alzheimer's disease.

Animals↗
PubMed2002

Ionic strength has a greater effect than does transmembrane electric potential difference on permeation of tryptamine and indoleacetic acid across Caco-2 cells.

The effects of transmembrane electric potential difference and ionic strength on the permeation of tryptamine and indoleacetic acid across a Caco-2 cell monolayer were examined. A decrease in the transmembrane electric potential difference caused by the addition of potassium ion to the transport buffer had no effect on the permeation rate of either compound. On the other hand, an increase in ionic strength resulted in a decrease in the permeation rate of tryptamine and an increase in the permeation rate of indoleacetic acid. The changes in the permeation rate with changes in the ionic strength were correlated with the membrane surface potential monitored by 1-anilino-8-naphthalenesulfonic acid (ANS), a fluorescent probe. We tested these effects using several other cationic and anionic compounds. These effects of ionic strength were found to be common to all drugs tested. The compound that showed a relatively lower permeation rate was given relatively stronger effect. The possibility of overestimation or underestimation caused by these effects should be considered when the permeation of an ionic compound is evaluated using a cell monolayer system.

Anilino Naphthalenesulfonates↗
PubMed2001

Two novel proaporphine-tryptamine dimers from Roemeria hybrida.

Roemeria hybrida yielded two novel proaporphine-tryptamine N-oxides, (-)-roehybridine alpha-N-oxide (1) and (-)-roehybramine beta-N-oxide (2). NMR data allowed a facile assignment of these proaporphine-tryptamine dimers into different stereochemical subgroups.

Alkaloids↗
PubMed1986

Quantification of tryptamine in brain using high-performance liquid chromatography.

The concentration of endogenously formed tryptamine in central nervous system tissue was determined after extraction into ethyl acetate, purification on a weak cation-exchange resin and analysis using high-performance liquid chromatography with fluorometric detection. Final chromatographic separation of this indoleamine was achieved using a muBondapak C18 reversed-phase column under isocratic conditions. Using this method, the concentration of tryptamine in the whole brain of normal rats was found to be 0.60 +/- 0.06 ng/g of tissue, while pretreatment with dl-p-chlorophenylalanine, tranylcypromine and l-tryptophan increased the concentration to 96.7 +/- 21.9 ng/g.

Acetylation↗
PubMed2000

2-Aryl tryptamines: selective high-affinity antagonists for the h5-HT2A receptor.

A series of 2-aryl tryptamines have been identified as high-affinity h5-HT2A antagonists. Structure-activity relationship studies have shown that h5-HT2A affinity can be attained via modifications to the tryptamine side chain and that selectivity over h5-HT2C and hD2 receptors can be controlled by suitable C-2 aryl groups.

Animals↗
PubMed2001

Heterocyclic derivatives of 2-(3,5-dimethylphenyl)tryptamine as GnRH receptor antagonists.

A series of heterocyclic 2-(3,5-dimethylphenyl)tryptamine derivatives was prepared and evaluated on a rat gonadotropin releasing hormone receptor assay. The carbon tether length and heterocyclic ring attached to the amino group of 2-(3,5-dimethylphenyl)tryptamine were varied. Several of these derivatives were potent GnRH antagonists with the most potent compound having an IC50 of 16 nM.

Animals↗
PubMed2001

2-(3,5-Dimethylphenyl)tryptamine derivatives that bind to the GnRH receptor.

A series of 2-(3,5-dimethylphenyl)tryptamine derivatives was prepared and evaluated on a rat gonadotropin releasing hormone receptor assay. Some para-substituents on the 4-phenylbutyl side chain attached to the tryptamine nitrogen led to compounds with potent GnRH receptor binding. The study has helped define structural requirements for GnRH receptor binding for the 2-aryltryptamine GnRH antagonists.

Animals↗
PubMed1979

Purification and properties of strictosidine synthetase (an enzyme condensing tryptamine and secologanin) from Catharanthus roseus cultured cells.

Strictosidine synthetase, which catalyzes the condensation of tryptamine with secologanin to form strictosidine (isovincoside), was purified 740-fold to homogeneity from cultured cells of Catharanthus roseus in 10% yield. The specific activity is 5.85 nkat/mg. The molecular weight as estimated by gel filtration is 38,000. The isoelectric point is 4.6. Apparent Km values for tryptamine and secologanin are 0.83 and 0.46 mM, respectively. The enzyme shows a broad pH optimum between 5.0 and 7.5. The product of the enzymic reaction is exclusively strictosidine, while no trace of its epimer vincoside can be detected. Sulfhydryl inhibitors have no effect on the enzyme. End products in the biosynthetic pathway of indole alkaloids such as ajmalicine, vindoline, and catharanthine do not inhibit the activity of strictosidine synthetase.

Carbon-Nitrogen Lyases↗
PubMed2005

Structural selection by microsolvation: conformational locking of tryptamine.

The conformational space of tryptamine has been thoroughly investigated using rotationally resolved laser-induced fluorescence spectroscopy. Six conformers could be identified on the basis of the inertial parameters of several deuterated isotopomers. Upon attaching a single water molecule, the conformational space collapses into a single conformer. For the hydrogen-bonded water cluster, this conformer is identified unambiguously as tryptamine A. In the complex, the water molecule acts as proton donor with respect to the amino group. An additional interaction with one of the aromatic C-H bonds selectively stabilizes the observed conformer more than all other conformers. Ab initio calculations confirm much larger energy differences between the conformers of the water complex than between those of the monomers.

Algorithms↗
PubMed1997

A novel series of 2,5-substituted tryptamine derivatives as vascular 5HT1B/1D receptor antagonists.

The design, synthesis, and activity of a novel series of 2,5-substituted tryptamine derivatives at vascular 5HT1B-like receptors is described. Several important auxiliary binding sites of the 5HT1B-like receptor have been proposed following various modifications to the 2-substituent and especially to the methylene- or ethylene-linked 5-side chain. Careful design of new molecules based on a proposed pharmacophoric model of the 5HT1B-like receptor has resulted in the discovery of ethyl 3-[2-(dimethylamino)ethyl]-5-[2-(2, 5-dioxo-1-imidazolidinyl)ethyl]-1H-indole-2-carboxylate (40), a highly potent, silent, competitive, and selective antagonist which shows affinity at the vascular 5HT1B-like receptors only. Changes to the size of the 2-ester substituent have a significant effect on affinity at the 5HT1B-like receptor and other receptors. Prudent placement of the carbonyl substituent in the heterocycle of the 5-side chain is crucial for good affinity and selectivity over the 5HT2A and other receptors. Several key structural and electronic features were identified which are crucial for producing antagonism within a tryptamine-based series. An electron deficient indole ring system appears essential in order to achieve antagonism, and this is achieved by the inclusion of electron-withdrawing groups at the 2-position of the indole ring. The molecule displacement within the receptor resulting from the inclusion of the bulky 2-substituents also enhances antagonism as this results in the removal of the pi electron density of the indole ring from the region of the receptor normally occupied by the indole ring of 5HT. There also appears to be a structural requirement on the side chain incorporating the protonatable nitrogen, and this is achieved by the inclusion of the bulky 2-ester group which neighbors the 3-ethylamine side chain.

Animals↗