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PubMed1995

Characterization of a postjunctional 5-HT receptor mediating relaxation of guinea-pig isolated ileum.

The 5-HT receptor mediating postjunctional relaxation of precontracted guinea-pig ileum has been characterized using several agonists and antagonists. Substance P precontracted tissues were potently relaxed by 5-HT (5-hydroxytryptamine, serotonin), 5-CT (5-carboxamidotryptamine) and several other indoles. The rank order of potency, with pEC50 values in parentheses, was 5-CT (7.6) > 5-methoxytryptamine (5.7) > 5-HT (5.5) > alpha-methyl-5-HT (4.7) > 2-methyl-5-HT (< 4.0) = tryptamine (< 4.0) = N,N-dimethyl-tryptamine (< 4.0) = N,N-dimethyl-5-HT (< 4.0) = dipropyl-5-CT (< 4.0) = sumatriptan (< 4.0). 8-OH-DPAT (8-hydroxy-2-(di-n-propylamino)-tetralin) acted as a potent (6.3), but partial, agonist with respect to 5-HT. The responses to 5-CT were antagonized by several compounds with the following rank order of affinity, with pKB values in parentheses: LSD (lysergic acid diethylamide; 8.1) = mesulergine (7.8) > methysergide (7.6) = spiperone (7.6) > clozapine (7.3) >> (-)-pindolol (< 6.0) > ketanserin (< 6.0) = ondansetron (< 6.0) = GR 113808 ([1-(2-methane-sulphonamido-ethyl)-piperidin-4-yl]-methyl-in dole-3- carboxylate maleate; < 6.0). The relaxant responses to 5-HT were also resistant to tetrodotoxin. These data are consistent with a functional 5-HT receptor, mediating relaxation of guinea-pig ileum, which exhibits an operational profile similar to that of the cloned guinea-pig 5-ht7 receptor. This study, therefore, provides evidence for a functional correlate of the 5-ht7 gene product.

5-Methoxytryptamine↗
PubMed1996

Structure-activity relationships for substrates and inhibitors of pineal 5-hydroxytryptamine-N-acetyltransferase: preliminary studies.

Tryptamine, (1-naphthyl)ethylamine and phenethylamine derivatives were tested as substrates of ovine pineal serotonin-N-acetyl transferase (5-HT-NAT), a key enzyme involved in the synthesis of melatonin. Almost all of the indole derivatives possessed affinity similar to that of tryptamine (Km = 0.05 mM), while the substituted naphthalene and phenyl derivatives were less potent. However, the Km values seem be influenced by the steric hindrance and polar properties of the substituent. Vmax values for the naphthyl and phenyl derivatives were generally 10-20-fold higher than those of the indole derivatives and no clear structure-activity relationship was observed. Melatonin and several bioisosteric derivatives were shown to be inhibitors of 5-HT-N-acetyltransferase. Preliminary data suggested that over the 5-50-microM concentration range, melatonin was a competitive inhibitor (IC50 = 10 microM) with a concentration-dependent inhibitory effect on its own synthesis in the pineal gland. However, the bioisosteric naphthalene derivatives were characterized instead as mixed inhibitors. (1-Napthyl)ethylacetamido, a putative melatoninergic antagonist, was also shown to be an inhibitor of 5-HT-N-acetyltransferase (IC50 = 8 microM) and is a promising tool for the regulation of melatonin synthesis and the understanding of its role.

Acetylation↗
PubMed1991

Tryptophanyl-tRNA synthetase in cell lines resistant to tryptophan analogs.

Bovine kidney cell lines resistant to tryptamine and tryptophanol (tryptophan analogs) were selected. The content of tryptophanyl-tRNA synthetase (WRS, EC 6.1.1.2) was assayed by measuring the binding of monospecific polyclonal antibodies to the 35S-labeled enzyme in detergent-soluble and -insoluble forms and measuring the enzyme activity. Both the enzyme content and activity were elevated in the resistant cells. As was found by immunoelectron microscopy, the initial and resistant cells contained WRS in most of their cellular compartments: on free polyribosomes, as large conglomerates in the cytoplasm, on polysomes bound to the rough endoplasmic reticulum membranes and to the outer nuclear membrane, on the cytoskeleton, and in the detergent-insoluble nuclear matrix. Immunochemically stained tangles of filaments were found in the resistant cells, but not in the control cells. WRS was less phosphorylated in the resistant than in the original Madin Darby bovine kidney cells. Karyological and morphometric analysis revealed that, in tryptamine-resistant cells, the marker acrocentric chromosome was longer and the frequency of its duplication rose to 96%. The results of this work indicate that the cultivated cells have become resistant to tryptophan analogs because of an elevated WRS concentration in the cells, possibly due to amplification of the WRS gene.

Animals↗
PubMed1983

Autoreceptor-mediated inhibition of 3H-5-hydroxytryptamine release from rat brain cortex slices by analogues of 5-hydroxytryptamine.

Rat brain cortex slices preincubated with 3H-5-hydroxytryptamine (3H-5-HT) were superfused with physiological salt solution containing paroxetine, an inhibitor of 5-hydroxytryptamine (5-HT) uptake. The effects of various indolethylamines on the electrically evoked tritium overflow (containing 66.3% unmetabolized 3H-5-HT) were investigated (the percentage of unmetabolized 3H-5-HT was not altered by the indolethylamines or metitepin). 6,7-Dihydroxytryptamine (6,7-DHT) did not affect the stimulation-evoked tritium overflow, whereas the latter was inhibited by the other tryptamine derivatives investigated; when the compounds were compared to each other on the basis of their inhibitory potencies the following rank order was obtained: unlabelled 5-HT greater than 5-methoxytryptamine greater than 4-HT greater than 6-HT greater than 5,6-DHT greater than tryptamine greater than 7-HT greater than 5,7-DHT. The inhibitory effects of these compounds were antagonized by metitepin. It is concluded that the indolethylamines inhibit the stimulation-evoked 3H-5-HT release by activating the presynaptic 5-HT autoreceptors on the 5-HT neurones of the rat brain cortex. Similarities may exist between these receptors and the postsynaptic 5-HT1 binding sites of this brain area.

5-Methoxytryptamine↗
PubMed1983

Determination of endogeneous indoleacetic acid and tryptophol in mouse brain by high performance liquid chromatography with fluorometric detection.

A simple and sensitive method using high performance liquid chromatography with fluorometric detection has been developed for the identification and quantitation of the endogeneous tryptamine metabolites, indoleacetic acid (IAA) and tryptophol (TOL) in the normal mouse brain. The limits of sensitivity are 5pg for both IAA and TOL. The extract procedure from the brain is only to deproteinize samples. The mean concentrations of IAA and TOL in the mouse brain are 8.99 +/- 0.31 ng/g and 3.56 +/- 0.21 ng/g respectively. The effects of pargyline and tryptamine on the levels of IAA and TOL were also studied.

Animals↗
PubMed1987

Effect of monofluoromethyldopa (MFMD) on trace amine levels.

The concentrations of the trace amines, m-tyramine, p-tyramine, phenylethylamine and tryptamine, were measured in the striatum of the brain and in the kidney of adult rats treated with alpha-monofluoromethyldopa (MFMD), an inhibitor of aromatic amino acid decarboxylase. While MFMD decreased the levels of all four amines in the kidney, only phenylethylamine and tryptamine levels were decreased in the striatum compared to control. Striatal p-tyramine levels were not affected, while striatal m-tyramine levels were increased by MFMD. When the rats were injected with a monoamine oxidase (MAO) inhibitor before MFMD administration, similar changes in striatal and kidney trace amine levels were observed compared to MFMD alone.

Animals↗
PubMed1975

Characterization of pancreatic islet monoamine oxidase.

Monoamine oxidase (MAO) is present in isolated islets of Langerhans of rabbits, golden hamsters, and rats. Tryptamine, tyramine, serotonin, and dopamine can serve as substrates for this enzyme. We compared the properties of islet and liver MAO in the rabbit. The Michaelis constant (K(m)) for tryptamine of islet MAO (6.5 times 10-5M) is greater than the K(m) of liver MAO (3 times 10-5M). The K(m) for tyramine of islet MAO (1.5 times 10-4M) is similar to the K(m) of liver MAO (1.8 times 10-4M). Islet MAO appeared to be more susceptible to heat inactivation (50 degrees C) than did liver MAO. This may be an artifact produced by the collagenase technique used in the preparation of the islets, as collagenase treatment of liver increased the thermal lability of the MAO in this tissue. Liver and islet MAO have a comparable sensitivity to MAO inhibitors such as clorgyline, deprenyl, tranylcypromine, pargyline, and harmine. The present report, along with previous reports that MAO inhibitors alter insulin secretion, suggests that islet MAO may modify insulin secretion.

Animals↗
PubMed1977

Effect of hyper- and hypothyroidism on platelet monoamine oxidase activity and serotonin metabolism.

We evaluated platelet monoamine oxidase (MAO) activity in 13 hyperthyroid and 9 hypothyroid patients. The platelet MAO activity of these patients did not differ from that of age- and sex-matched euthyroid control subjects. Nineteen hyperthyroid and twelve hypothyroid subjects had serum serotonin concentrations similar to those of age- and sex-matched euthyroid control subjects. We also determined the urinary excretion of 5-hydroxy-indoleacetic acid (5-HlAA), serotonin, tryptamine, and tyramine in five hyperthyroid and four hypothyroid subjects. Two hyperthyroid patients had increased tyramine excretion; one of these patients also had increased tryptamine excretion. Three hypothyroid patients and one hyperthyroid patients had slightly decreased serotonin excretion. Both the hyper- and the hypothyroid subjects had normal urinary 5-HIAA excretion. There was no relationship between platelet MAO activity and monoamine excretion in the patients with thyroid dysfunction. We conclude that there is no systematic change in platelet MAO activity or serum serotonin concentration in patients with hyper- or hypothyroidism.

Adult↗
PubMed1985

Effects of ketanserin on neuronal responses to serotonin in the prefrontal cortex, lateral geniculate and dorsal raphe nucleus.

The ability of the putative serotonin2 (5-HT2) antagonist ketanserin, to alter serotonin (5-HT)-induced responses in cell firing was examined in the prefrontal cortex, the lateral geniculate nucleus and the dorsal raphe nucleus of the rat by microiontophoretic extracellular single unit recording techniques. In the prefrontal cortex, ketanserin failed to antagonize the inhibitory effects of 5-HT recorded in cerveau isolé or preparations anesthetized with chloral hydrate (pure excitatory responses to 5-HT were not observed in either of these preparations). Paradoxically, the inhibitory response produced by 5-HT (but not gamma-aminobutyric acid, tryptamine or norepinephrine) was potentiated, even in cells where ketanserin alone did not alter spontaneous firing rates. The systemic administration of ketanserin (5 mg/kg, i.p.) had effects similar to those observed in the microiontophoretic experiments in the prefrontal cortex. In the dorsal raphe nucleus of animals anesthetized with chloral hydrate, ketanserin neither attenuated nor potentiated the inhibition of serotonergic neurons by 5-HT. In the lateral geniculate nucleus, as in the prefrontal cortex, ketanserin potentiated rather than attenuated, the inhibitory effect of 5-HT. Ketanserin was found to attenuate the excitatory responses produced by norepinephrine, an alpha 1-adrenoceptor-mediated response, in the lateral geniculate nucleus. The observed potentiation by ketanserin of inhibitory responses to 5-HT but not those of gamma-aminobutyric acid, tryptamine or norepinephrine, recorded in the prefrontal cortex, may be consistent with the proposed interaction between ketanserin and a specific 5-HT2 binding site.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1980

A sensitive and rapid fluorimetric assay for monoamine oxidase utilizing high pressure liquid chromatography.

A rapid and sensitive assay for the measurement of monoamine oxidase (MAO) activity was developed. This method utilizes high pressure liquid chromatography with fluorescence excitation at 280 nm and detection of 330 nm at pH 5.0 of indoleacetic acid and 5-hydroxyindoleacetic acid, the deaminated products of two substrates for MAO, tryptamine, and serotonin, respectively. The assay allows for the complete separation of metabolites from either of the two substrates. The method has been used to determine MAO activity in the frontal cortex and caudate nucleus of rat brain using tryptamine and serotonin as substrates. The ease and rapidity of this assay make it sutable for use where routine enzyme determinations are required.

Animals↗
PubMed1984

Displacement of serotonin from binding sites in rat cortex: the effects of biogenic "trace" amines.

The concentrations for 50 percent inhibition of binding (IC50's) to specific in vitro serotonin binding sites (5-HT1 and 5-HT2) of rat cerebral cortex were determined for the trace amines 2-phenylethylamine, m- and p-tyramine, tryptamine, and (+)- and (-)- alpha-methyltryptamine. Tryptamine gave an IC50 of 66.7 +/- 4.8 nM (n = 7) at the 5-HT1 site and an IC50 of 3.85 +/- 0.16 microM (n = 7) for the 5-HT2 binding site. The IC50 values for all the other compounds were in the micromolar range and were different at the two binding sites except for p-tyramine (IC50, 5-HT1 = IC50, 5-HT2 = 17 microM. The trace amines may have different functional roles as evidenced by their different degrees of displacement of serotonin at 5-HT1 and 5-HT2 binding sites in the brain.

Animals↗
PubMed1987

Counteraction of the genotoxicity of some cooked-food mutagens by biogenic amines.

The biogenic amines tryptamine, 5-hydroxytryptamine, tyramine and histamine were assessed for their abilities to modify the genotoxicity of the cooked-food mutagens IQ, MeIQ, MeIQx, Trp-P-1 and Trp-P-2. These measurements were made using a bacterial mutation assay with hepatic fractions from either SWR mice or DSN Syrian hamsters as the activating system and Salmonella typhimurium TA98 as the indicator organism. Although histamine had very little effect on the genotoxicity of these mutagens, the other amines reduced genotoxicity, with tryptamine and 5-hydroxytryptamine exerting the greatest effect. Generally the amines exhibited greater potency when S-9 fractions from mice rather than from hamsters were used.

Animals↗
PubMed1996

Absence of alkaloids in Psychotria carthagenensis Jacq. (Rubiaceae).

Psychotria viridis and P. carthagenensis are often discussed in relation to the hallucinogenic beverage Ayahuasca, used for religious, medicinal and social purposes. The significance of including Psychotria species in this beverage has been understood on the basis of substantial amounts of tryptamine alkaloids detected on leaves of both P. viridis and P. carthagenensis. Nevertheless, there is a long lasting debate over the identification of which Psychotria species are actually traditionally employed. We here report that a P. carthagenensis leaf ethanol extract was found to be devoid of alkaloids. The extract significantly decreased mice body temperature (350 and 500 mg/kg). Toxicity assessment revealed that the extract induced sedation and slight ptoses (75% of animals treated with 1000 mg/kg). Lethality was not observed within 48 h. The data indicate that P. carthagenensis does have bioactive compound(s), possibly active at the central nervous system, but unlikely to be tryptamine alkaloids as in the case of P. viridis. Therefore, if P. carthagenensis is indeed used by ayahuasqueros, its chemical and pharmacological significance have yet to be elucidated.

Analysis of Variance↗
PubMed2005

Major depression and the synthetic enhancer substances, (-)-deprenyl and R-(-)-1-(benzofuran-2-yl)-2-propylaminopentane.

Because of the high number of therapy-resistant depressions and the growing number of suicides, there is still a great need for the development of antidepressants with a new pharmacological spectrum. The finding that phenylethylamine and tryptamine are endogenous enhancers of the impulse propagation mediated release of catecholamines and serotonin in the brain, and the development of synthetic enhancer substances opened the possibility to stimulate catecholaminergic and serotonergic neurons in the brain stem via a previously unknown mechanism. (-)-Deprenyl, a prototype of the phenylethylamine-derived synthetic enhancer substances, stimulates the catecholaminergic neurons in the brain but is almost ineffective on the serotonergic neurons. R-(-)-1-(benzofuran-2-yl)-2-propylaminopentane, (-)-BPAP, the recently developed tryptamine-derived selective synthetic enhancer substance, is a hundred times more potent enhancer of the catecholaminergic neuronal activity than (-)-deprenyl, and is also a highly potent stimulant of the serotonergic neurons. Evaluation of the peculiar pharmacological profile, the high potency and unusual safeness and tolerability of (-)-BPAP cherish the hope that this compound by itself and in combination with uptake inhibitors may improve the effectiveness of drug therapy in major depression and diminish the number of therapy resistant cases.

Animals↗
PubMed1976

Nucleic acids-protein interactions. Conformational changes induced by the binding of aromatic amines to polyadenylic acid.

The binding of Tryptamine, Serotonine, Phenylethylamine and Histamine to poly(A) in its single stranded form at pH 7 leads to a decrease of its circular dichroism (C.D) amplitude without any appreciable alteration of the shape of the C.D. spectrum. The magnitude of the effect depends on the size of the aromatic ring and decreases in the order : tryptamine greater than tyramine greater than phenylethylamine greather than histamine. A method is described which allows the calculation of association constants from C.D. data. The C.D. amplitude decreases linearly with concentration of bound molecules. Binding of aromatic amines to poly(A) leads to a change in the proton chemical shifts of both the amine and the poly(A) protons. Quantitative analysis of P.M.R. data demonstrates that the shifts of poly(A) protons are linearly related to the concentration of bound molecules.

Amines↗
PubMed1997

Characterization of the role of side-chain interactions in the binding of ligands to apo trp repressor: pH dependence studies.

The pH dependence of the association of apo trp repressor with the series of ligands, tryptophan, tryptamine, indole propionic acid (IPA), and trans-beta-indole acrylic acid (IAA), has been studied using fluorescence titrations and isothermal titration microcalorimetry (ITC). The purpose of such a comparison of ligands and the pH dependency studies is to reveal the role played by the side-chain functional groups in the energetics of the binding of the ligands to the protein. We find that, whereas the binding of tryptamine and IPA have essentially no pH dependence between pH 6 and 10, the binding of tryptophan and IAA depends on pH. For IAA, the affinity drops between pH 6 and 10, consistent with a shift in pKa of some group on the protein from a value of pKa 7.4 to 7.9 upon binding of this ligand. The affinity of IAA also drops below pH 5, but shows saturable binding at pH 2-3, where the protein has previously been found to exist as a partially folded monomeric state. For tryptophan, the pH dependence data indicate that the equilibrium is complicated. We present a model to describe the data in which the alpha-ammonium group of tryptophan has its pKa shifted upward upon binding (i.e. preferential binding of the protonated form of this functional group) and in which the pKa of an unknown group on the protein also has its pKa increased.

Bacterial Proteins↗
PubMed1979

Longitudinal urinary trace amine excretion in a human male.

The urinary excretion of a beta-phenylethylamine (PE), m-tyramine (mTA), p-tyramine (pTA) and tryptamine (TR) in their unconjugated (free) and conjugated (except tryptamine) forms, was examined in a male human subject over a total period of 28 days. The average excretion values were (in microgram per 24 h, mean +/- standard error): PE, free 3.19 +/- 0.21, conjugated 6.85 +/- 0.52, mTA, free 98.0 +/- 2.2, conjugated 106.1 +/- 18.6; pTA, free 427 +/- 12, conjugated 571 +/- 142; and TR, free 79.4 +/- 2.8. This data, when considered along with other published information, permits the suggestion that probably mTA and pTA in the unconjugated form are exclusively formed endogenously; whether or not this also pertains to PE and TR is less clear. In all cases, the conjugated amines derive from both exogenous and endogenous sources.

Humans↗
PubMed1985

Human brain monoamine oxidase type B: mechanism of deamination as probed by steady-state methods.

Recently, evidence has been published which suggests that [Husain, M., Edmondson, D. E., & Singer, T.P. (1982) Biochemistry 21, 595-600] monoamine oxidase [amine:oxygen oxidoreductase (MAO), EC 1.4.3.4] deaminates phenylethylamine and benzylamine via two distinct kinetic pathways which involve either binary or ternary complex formation, respectively. These conclusions were drawn largely from stopped-flow kinetic analysis performed on purified enzyme removed from its native membrane and in the presence of the inhibitory detergent Triton X-100. In this study, d-amphetamine and alternative substrates were used as steady-state probes of the kinetics of deamination by the B form of human brain MAO using native membrane-bound enzyme. Initial velocity studies showed mixed-type patterns for amphetamine inhibition of phenylethylamine, tryptamine, and tyramine when either amine or oxygen was the varied substrate. Slope and intercept vs. amphetamine concentration replots were linear in all cases except for phenylethylamine (hyperbolic); Ki values obtained from linear replots of slope or intercept values were comparable. In contrast, amphetamine was a competitive inhibitor of benzylamine deamination when amine concentration was varied and uncompetitive when oxygen concentration was varied; slope and intercept replots were linear for both. When benzylamine was the alternative substrate inhibitor and tyramine and tryptamine deamination was measured, mixed-type inhibition patterns were obtained when either amine or oxygen concentration was varied; replots of slope and intercept were linear in all cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain↗