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PubMed1983

Analysis of the contractile response to serotonin and tryptamine of isolated dog cerebral, femoral and mesenteric arteries.

In helically-cut strips of cerebral arteries isolated from dogs, serotonin, tryptamine, 5-hydroxytryptophan and tryptophan caused a dose-related contraction. The potency was in the order of serotonin greater than tryptamine much greater than 5-hydroxytryptophan = tryptophan. In femoral arterial strips, only serotonin and tryptamine produced contractions. In cerebral arteries, the dose-response curve for serotonin was shifted to the right and downward by treatment with cinanserin, whereas in femoral and mesenteric arteries, the curves were shifted to the right. The contractile response of cerebral arteries to tryptamine was attenuated by cinanserin in concentrations above 10(-7) M; however, 10(-5) M was required to significantly reduce the response of femoral arteries. Phentolamine reduced the contractile response of femoral arteries to tryptamine, but not the response of cerebral arteries. It may be concluded that the different antagonism of cinanserin against the serotonin action on cerebral and femoral arteries is due to the ability of high concentrations of serotonin to induce relaxations of cerebral but not femoral arteries or to the different nature of receptors. Tryptamine appears to elicit contractions of cerebral arteries via a stimulation of tryptamine receptors, but elicit those of femoral arteries via stimulation of both alpha-adrenergic and tryptamine receptors. Whether or not receptors for serotonin and tryptamine are the same was not determined.

5-Hydroxytryptophan↗
PubMed1985

Relationship between serotonin and tryptamine receptors in the rat stomach fundus.

Tryptamine and serotonin (5-HT) are relatively potent contractile agonists in the rat fundus, a tissue in which contraction to 5-HT is not mediated by interaction with 5-HT1 or 5-HT2 receptors. The identification of [3H]tryptamine binding sites in the brain and fundus that show high affinity for certain beta-carbolines raised the possibility that 5-HT and tryptamine may be interacting with a similar receptor that is best described as a tryptaminergic receptor in the fundus. The affinity of five 5-HT receptor antagonists, ketanserin, metergoline, 1-(1-naphthyl)piperazine, LY154930 and LY175041 was similar when 5-HT or tryptamine was the agonist, indicating that 5-HT and tryptamine are interacting with the same receptor in the fundus. Furthermore, maximum contractile response to both 5-HT and tryptamine was reduced to the same extent by the calcium channel blocker, diltiazem, and by the calmodulin inhibitor, trifluoperazine. Inasmuch as diltiazem and trifluoperazine did not similarly inhibit contraction to agents interacting with other receptors (i.e., carbamylcholine), these data are consistent with the contention that 5-HT and tryptamine are interacting with the same receptor in the fundus. Consistent with this conclusion is the observation that affinity of the beta-carbolines, harmaline and harmine was also similar when tryptamine or 5-HT was used as the agonist. However, affinity of the beta-carbolines for the tryptamine/5-HT receptor in the fundus was dramatically lower than reported for [3H]tryptamine binding sites in brain membranes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Alterations in brain 5HT and tryptamine content during indoleamine-induced myoclonus in guinea pigs.

L-5-Hydroxytryptophan (5HTP) (with or without carbidopa pretreatment), L-tryptophan (plus pargyline pretreatment), or tryptamine (plus pargyline pretreatment) all induced dose-dependent myoclonus in guinea pigs. At the time of maximal behavioural response animals were killed for determination of brain indoleamine content. Administration of 5HTP (50-200 mg/kg) to naive guinea pigs, or of 5HTP (20-80 mg/kg) to carbidopa- (25 mg/kg 1 hr previously) pretreated animals, markedly elevated brain 5-hydroxytryptamine (5HT) concentrations but depressed whole brain tryptamine content. L-Tryptophan (50-200 mg/kg) administration to pargyline- (75 mg/kg 30 min previously) pretreated animals also increased cerebral 5HT levels. L-Tryptophan (200 mg/kg plus pargyline), elevated whole brain tryptamine content. Administration of tryptamine (40 mg/kg) to pargyline-pretreated guinea pigs caused a small increase in brain 5HT levels, but markedly elevated cerebral tryptamine content. 5HT appears to be the indoleamine mainly responsible for 5HTP-induced myoclonus but tryptamine predominates in tryptamine-induced myoclonus. Both 5HT and tryptamine may contribute to myoclonus induced by L-tryptophan.

5-Hydroxytryptophan↗
PubMed1986

Tryptamine depletion in the rat striatum following electrolytic lesions of the substantia nigra.

Tryptamine is an indolic compound that occurs naturally in the mammalian central nervous system. To test whether tryptamine-containing neurons are present in the nigrostriatal system, we investigated effects of unilateral electrolytic lesions of the substantia nigra on striatal tryptamine concentrations. Determinations were made 7 days after lesioning. Nigral lesions resulted in an ipsilateral reduction in accumulation of striatal tryptamine observed after monoamine oxidase inhibition. As tryptamine formation is dependent on the activity of the enzyme L-aromatic acid decarboxylase (L-AAD), which is present in monoamine-containing neurons, the reduction in accumulation of tryptamine after nigral lesions may be secondary to enzyme loss with the degeneration of dopamine-containing neurons. Nevertheless, failure to observe decreases in the accumulation of tryptamine after raphé lesions, which deplete striatal 5-HT and L-AAD, indicates that tryptamine may be associated specifically with neurons in the nigrostriatal system.

Animals↗
PubMed1987

[3H]tryptamine binding sites of rat cerebral cortex: pharmacological profile and plasticity.

Equilibrium saturation analysis of the binding of [3H]tryptamine to membranes from the cerebral cortex of the rat at 0 degrees C indicated that [3H]tryptamine bound to a single class of high affinity binding sites (Kd = 1.29 +/- 0.13 nM). The binding of [3H]tryptamine was potently inhibited by tryptamine itself, beta-carboline, tetrahydro-beta-carboline and several beta-phenylethylamine derivatives. Structure-activity relationships of the beta-phenylethylamines tested showed that substitutions in para-position were the most potent with the following rank order of potency H less than OH less than Cl less than OCH3. Although chronic treatment with parachlorophenylalanine did not affect the parameters of the binding of [3H]tryptamine to cerebral cortical membranes of the rat, chronic treatment with clorgyline and deprenyl resulted in a 49% decrease in the density of binding sites for [3H]tryptamine, with no change in Kd. This modulation of the binding of [3H]tryptamine lends support to the proposal that binding sites for [3H]tryptamine could represent a specific class of receptors in the CNS. As such, the structure-activity relationships revealed within and between the various families of compounds tested provides useful information for the development of new chemical tools as potential agonists and/or antagonists at these sites.

Animals↗
PubMed1997

Evaluation of tryptamine in an impinger and on XAD-2 for the determination of hexamethylene-based isocyanates in spray-painting operations.

Tryptamine was evaluated as a reagent for derivatizing hexamethylene diisocyanate (HDI) monomer and oligomers during actual spray-painting operations. In one side-by-side sampling study, an impinger filled with 1-(2-methoxyphenyl)piperazine in toluene was compared with a second impinger filled with tryptamine in dimethyl sulfoxide (DMSO). The amount of HDI monomer obtained was below the limit of quantification for both impingers. The amount of HDI oligomer obtained when using 1-(2-methoxyphenyl)piperazine in toluene was comparable to the amount obtained when using an impinger filled with tryptamine in DMSO. In a second side-by-side sampling study, a tryptamine-coated XAD-2 resin was used as a sorbent. The relative collection efficiency of the tryptamine-coated XAD-2 resin was on average 60% of the value obtained using an impinger filled with tryptamine in DMSO. The results indicate that using an impinger filled with tryptamine in DMSO gives higher concentrations of isocyanate than a tryptamine-coated XAD-2 sorbent for HDI monomer and oligomer.

Dimethyl Sulfoxide↗
PubMed1994

Tryptamine induces phosphoinositide turnover and modulates adrenergic and muscarinic cholinergic receptor function in cultured cerebellar granule cells.

Tryptamine dose-dependently increased phosphoinositide (PI) hydrolysis by approximately fourfold in primary cultures of rat cerebellar granule cells (EC50 = 56 microM). The PI response stimulated by tryptamine was dependent on the presence of extracellular Ca2+ and Na+. Tryptamine-induced PI breakdown could be partially inhibited by pretreatment with 4 beta-phorbol 12-myristate 13-acetate but not pertussis toxin. The presence of tryptamine markedly attenuated PI responses induced by norepinephrine (NE) and carbachol, with no apparent effect on the responses to 5-hydroxytryptamine and glutamate. The inhibition of NE- and carbachol-induced PI turnover by tryptamine was dose dependent with IC50 values of approximately 0.4 and approximately 2.5 mM, respectively. Pretreatment of cells with tryptamine (0.5 mM) also attenuated NE- and carbachol-induced PI turnover, but failed to affect 5-hydroxytryptamine- and glutamate-induced responses. Furthermore, ketanserin, atropine, and prazosin did not have any effect on inositol phosphate formation induced by tryptamine. These observations indicate that tryptamine markedly increased Ca(2+)- and Na(+)-dependent PI turnover in cerebellar neurons and selectively inhibited NE- and carbachol-induced PI hydrolysis.

Animals↗
PubMed2003

The relative contribution of monoamine oxidase and cytochrome p450 isozymes to the metabolic deamination of the trace amine tryptamine.

Tryptamine is a trace amine in mammalian central nervous system that interacts with the trace amine TA(2) receptor and is now thought to function as a neurotransmitter or neuromodulator. It had been reported that deamination of tryptamine to tryptophol was mediated by CYP2D6, a cytochrome P450 that is expressed in human brain, suggesting that tryptamine may be an endogenous substrate for this polymorphic enzyme. We were unable to confirm this report and have reinvestigated tryptamine metabolism in human liver microsomes (HLM) and in microsomes expressing recombinant human cytochrome P450 and monoamine oxidase (MAO) isozymes. Tryptamine was oxidized to indole-3-acetaldehyde by HLM and recombinant human MAO-A in the absence of NADPH, and indole-3-acetaldehyde was further reduced to tryptophol by aldehyde reductase in HLM in the presence of NADPH. Steady-state kinetic parameters were estimated for each reaction step by HLM and MAO-A. The CYP2D6 substrates bufuralol and debrisoquine showed strong inhibition of both tryptophol production from tryptamine in HLM and the formation of indole-3-acetaldehyde from tryptamine catalyzed by recombinant MAO-A. Anti-CYP2D6 monoclonal antibody did not inhibit these reactions. Pargyline, a nonselective MAO inhibitor, did not show cross inhibition to debrisoquine 4-hydroxylation and dextromethorphan O-demethylation by HLM and recombinant CYP2D6 enzyme. This is the first unequivocal report of the selective conversion of tryptamine to tryptophol by MAO-A. CYP2D6 does not contribute to this reaction.

Cytochrome P-450 CYP2D6↗
PubMed1987

[3H]tryptamine binding to reconstituted fraction of acidic lipids.

The possible involvement of sulphatides (CS), phosphatidylserine (PS) and phosphatidylinositol (PI) in [3H]tryptamine binding to various reconstituted fractions of these acidic lipids was examined by Sephadex LH20 column chromatography. The results indicated that each of the four systems, PS, PS-CS, PS-PI and PS-CS-PI, had the same binding capacity for [3H]tryptamine, whereas other systems (CS, PI and CS-PI systems) had no binding capacity. Furthermore, competitive inhibition experiments revealed that among these four reconstituted systems, the PS-CS system exhibited the highest affinity for 5-methoxytryptamine. Kinetic studies suggested that at least two binding components (or sites) are implicated in the binding of [3H]tryptamine to the reconstituted system of PS and CS with apparent KD values of 3 and 10 nM. Displacement studies with various compounds indicated that only tryptamine and 5-methoxytryptamine inhibited the [3H]tryptamine binding to this fraction, while other indoleamine analogues and neurotransmitters had no effect. In addition, we subjected whole rat brain synaptic plasma membranes to treatment with several kinds of lipid-modifying reagents and examined the [3H]tryptamine binding capacities of the membranes by a radioreceptor-binding assay. [3H]Tryptamine binding was decreased by treatment with Azure A and phospholipase A2, while phospholipase D had no effect. All these observations led to the inference that PS and CS may be involved in the tryptamine binding activities as recognition sites.

Animals↗
PubMed2007

Tryptamine induces tryptophanyl-tRNA synthetase-mediated neurodegeneration with neurofibrillary tangles in human cell and mouse models.

The neuropathological hallmarks of Alzheimer's disease (AD) and other taupathies include neurofibrillary tangles and plaques. Despite the fact that only 2-10% of AD cases are associated with genetic mutations, no nontransgenic or metabolic models have been generated to date. The findings of tryptophanyl-tRNA synthetase (TrpRS) in plaques of the AD brain were reported recently by the authors. Here it is shown that expression of cytoplasmic-TrpRS is inversely correlated with neurofibrillary degeneration, whereas a nonionic detergent-insoluble presumably aggregated TrpRS is simultaneously accumulated in human cells treated by tryptamine, a metabolic tryptophan analog that acts as a competitive inhibitor of TrpRS. TrpRSN- terminal peptide self-assembles in double-helical fibrils in vitro. Herein, tryptamine causes neuropathy characterized by motor and behavioral deficits, hippocampal neuronal loss, neurofibrillary tangles, amyloidosis, and glucose decrease in mice. Tryptamine induced the formation of helical fibrillary tangles in both hippocampal neurons and glia. Taken together with the authors' previous findings of tryptamine-induced nephrotoxicity and filamentous tangle formation in kidney cells, the authors' data indicates a general role of tryptamine in cell degeneration and loss. It is concluded that tryptamine as a component of a normal diet can induce neurodegeneration at the concentrations, which might be consumed along with food. Tryptophan-dependent tRNAtrp aminoacylation catalyzed by TrpRS can be inhibited by its substrate tryptophan at physiological concentrations was demonstrated. These findings indicate that the dietary supplementation with tryptophan as a tryptamine competitor may not counteract the deleterious influence of tryptamine. The pivotal role of TrpRS in protecting against neurodegeneration is suggested, providing an insight into the pathogenesis and a possible treatment of neurodegenerative diseases.

Animals↗
PubMed1998

Direct fluorometry of phase-extracted tryptamine-based fast quantitative assay of L-tryptophan decarboxylase from Catharanthus roseus leaf.

An assay for the enzyme L-tryptophan decarboxylase (TDC; EC 4.1.1.28) is described. It is based on direct fluorometry of the enzymatic reaction product (tryptamine) selectively recovered in ethyl acetate from the reaction mixture. Catalytically formed tryptamine from tryptophan in the incubation mixture is selectively (free from tryptophan) physically separated as ethyl acetate solution under basic (pH > or = 11) conditions and subjected to direct fluorescence measurement in the organic solvent using a spectrofluorometer with excitation and emission wavelengths of 280 and 350 nm, respectively. Tryptamine production rate was quantitated from the luminescence response curve of tryptamine drawn under similar extraction and measurement conditions. Luminescence calibration curves were drawn for tryptamine in aqueous (water or buffer system) as well as in organic solvent as recovered from the varied aqueous solution conditions including those similar to the enzyme incubation mixture. The luminescence calibration graphs were linear for at least 0.5 to 10 microM tryptamine. The examination of interassay variations and the comparative magnitude of fluorescence response allowed to infer that a satisfactory and sufficient sample luminescence response was retained under the varied conditions including those akin to the enzymatic assay mixture, allowing adaptation of the fluorometry for the TDC activity quantitation. The assay was found to follow the proportionality principle of product formation with respect to catalytic reaction time as well as protein concentration in the assay mixture using Catharanthus roseus leaf crude homogenate as well as the enzyme preparation at different states of purity. The rate of tryptamine formation under the catalytic conditions was linear for at least 1 h at 30 degrees C. Though the assay has been demonstrated to use the C. roseus leaf as the enzyme source, it should be equally applicable to other plant and nonplant sources. The merits and precautions of the protocol have been discussed.

Alkalies↗
PubMed1987

Formation of a beta-carboline (1,2,3,4-tetrahydro-1-methyl-beta-carboline-1-carboxylic acid) following intracerebroventricular injection of tryptamine and pyruvic acid.

Tritium labelled 1-carboxy-tetrahydroharman was identified in rat brain following i.c.v.-injection of [3H]tryptamine and pyruvic acid. The animals had been treated with the MAO inhibitor pargyline (40 mg/kg) 30 min before i.c.v. injection. Under these conditions, only trace amounts of [3H]indole acetic acid could be detected in the brain. The formation of 1-CTHH was time-dependent. Five minutes following the i.c.v. injection, approximately 0.45% of the administered tryptamine was converted into 1-CTHH and 23% were still unchanged. The amount of the radioactive 1-CTHH increased slightly within 1 h (0.8%; [3H] tryptamine: 6%). Pretreatment of the rats with high doses of pargyline (75 mg/kg; 90 min before i.c.v. injection) prevented the formation of both [3H]1-CTHH and [3H]indole acetic acid (IAA) suggesting that high doses of pargyline inhibit the formation of 1-CTHH. As control for a possible non-enzymatic formation of 1-CTHH, [3H]tryptamine and various concentrations of pyruvic acid were incubated in phosphate buffer at pH 7.4. 1-CTHH was not detected under these conditions. However, the formation of 1-CTHH was observed at high pyruvic acid concentrations (final concentration = 100 mM) and low pH values (less than pH4). To support the assumption that the observed condensation of both precursors to 1-CTHH occurred intracellularly, the metabolism of tryptamine was studied. Two minutes after i.c.v. injection of [3H]tryptamine approximately 4% of the injected dose remained unchanged and 10% were metabolized to [3H]IAA. These findings suggest a rapid disappearance of [3H]tryptamine from the cerebrospinal fluid as well as a rapid penetration into the cerebral tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Inhibitory effects of tryptamine on tolbutamide-induced hypoglycemia in mice: mediation by 5-HT receptors.

Effects of tryptamine on tolbutamide-induced hypoglycemia were investigated in mice. Tryptamine significantly inhibited hypoglycemia elicited by tolbutamide. The inhibitory effects of tryptamine were strongly blocked by the 5-HT1 and 5-HT2 receptor antagonist methysergide and the 5-HT2 receptor antagonist ketanserin, while the 5-HT3 receptor antagonist ICS 205-930 was without effect. Tryptamine induced hyperglucagonemia in tolbutamide-treated mice, and this effect elicited by tryptamine was strongly inhibited by the 5-HT2 receptor antagonist ketanserin. These results suggest that the inhibitory effects of tryptamine on tolbutamide-induced hypoglycemia are mediated by 5-HT2 receptors and that tryptamine is involved in glucagon release.

Animals↗
PubMed1992

Membrane-potential-dependent uptake of tryptamine by rat intestinal brush-border membrane vesicles.

The effect of membrane potential on the uptake of tryptamine, an organic cation, by rat intestinal brush-border membrane vesicles was studied. In the presence of an outwardly directed H(+)-gradient, the initial uptake of tryptamine was stimulated remarkably and the overshoot phenomenon was observed. In contrast, the uptake was depressed by an inwardly-directed H(+)-gradient. The effect of H(+)-gradient on the uptake of tryptamine was maintained in the presence of FCCP, whereas it vanished when voltage-clamped vesicles were used. Moreover, the uptake of tryptamine was linearly augmented with increase of the valinomycin-induced inside-negative K+ diffusion potential. These results suggest that tryptamine is taken up into intestinal brush-border membrane vesicles depends upon the ionic diffusion potential. The effect of several indole derivatives and amine compounds on the uptake of tryptamine was also examined. The uptake of tryptamine was inhibited by all amine compounds used, but anionic and zwitterionic compounds had no effect, suggesting that these amines interact on brush-border membrane and cause an inhibitory effect.

Amines↗
PubMed1987

Down-regulation of tryptamine receptors following chronic administration of clorgyline.

Chronic treatment with clorgyline, a type A monoamine oxidase (MAO) inhibitor (1 mg/kg/day for 11 days), reduced the number (Bmax) but not the affinity (Kd) of [3H]tryptamine binding sites in rat frontal/parietal cortical membranes. Binding was reduced for at least 36 days following the last injection. The reduction in [3H]tryptamine binding was dose-related and appeared to be maximal following a daily dose of 3 mg/kg. Chronic treatment with deprenyl, a type B MAO inhibitor (1 mg/kg/day for 11 days), did not affect [3H]tryptamine binding. Acute clorgyline administration (11 mg/kg) also had no effect. These data suggest that [3H]tryptamine binds to neurotransmitter receptors for tryptamine since mere chemical recognition sites would not be expected to be modulated by chronic drug treatment. Also, since [3H]tryptamine binding was down-regulated by a type A, but not a type B, MAO inhibitor, tryptamine may be selectively metabolized by type A MAO in vivo.

Animals↗
PubMed1987

Pharmacological analysis of the variation in behavioural responses to tryptamine in five strains of mice.

The effects of tryptamine on behaviour were studied in five strains of mice. There were significant strain differences in the intensity of the 5-HT syndrome (head weaving and hindlimb abduction) and head twitch responses. The intensity of the 5-HT syndrome correlated significantly with the brain tryptamine content, although the occurrence of head twitch was unrelated. The 5-HT2 receptor antagonist, ketanserin, antagonized the head twitch responses elicited by tryptamine without affecting the head weaving or hindlimb abduction. Metergoline, an antagonist of both the 5-HT1 and 5-HT2 receptors, strongly inhibited both the 5-HT syndrome and the head twitch responses in all five strains. [3H]5-HT and [3H]ketanserin binding in the frontal cortex of the five strains of mice was also studied. The number of [3H]5-HT binding sites did not differ among the five strains of mice although there was a noticeable difference in the number of [3H]ketanserin binding sites. These results suggest that the 5-HT syndrome and the head twitch responses induced by tryptamine are linked separately with the 5-HT1 and 5-HT2 receptors, respectively. The strain differences in the tryptamine-induced 5-HT syndrome can be explained by the different levels of brain tryptamine. The differences in the head twitch responses in the mice are probably derived from the differences in the 5-HT2 receptor binding sites in the brain and the content of brain tryptamine.

Animals↗
PubMed1982

A comparison of the responses of cortical neurones to iontophoretically applied tryptamine and 5-hydroxytryptamine in the rat.

Tryptamine, applied iontophoretically to cortical neurones, had predominantly depressant effects. In contrast 5-hydroxytryptamine (5HT) exhibited excitatory effects on many neurons. On over 40% of neurones responsive to both 5HT and tryptamine the amines had opposite effects. A comparison of the magnitude of the depressant responses revealed that tryptamine was a much more effective depressant agent than 5HT. The iontophoretic transport numbers for 5HT and tryptamine were similar, indicating that the apparently greater potency of tryptamine was genuine. Electrolytic lesions of the medial forebrain bundle did not alter the relative effects of the amines, suggesting that there was a post-synaptic origin for the difference. Finally, the indoleamine antagonist metergoline was found to block selectively the tryptamine responses with little effect on 5HT responses, at low concentrations. The results suggest that tryptamine may possess post-synaptic effects unrelated to direct agonist actions at 5HT receptors.

Animals↗
PubMed1998

The indole alkaloid tryptamine impairs reproduction in Drosophila melanogaster.

The plant-produced indole alkaloid tryptamine is one of a large array of neuroactive substances that may affect insect behavior, development, and physiology. We tested the role of tryptamine on insect reproduction using the fruit fly, Drosophila melanogaster (Meigen), as a model system. Measurements were made of reproductive success, oviposition rate, and preadult survival of insects on artificial diets containing tryptamine, its precursor tryptophan, as well as glycine and serotonin (5-hydroxytryptamine). Drosophila reproduction was reduced to 15% of controls when adult insects mated and the young were allowed to develop on medium containing 75 mM tryptamine. Tryptamine-induced depression in reproductive success was due to decreased oviposition rate and preadult survival. Serotonin, but not tryptophan or glycine, also reduced oviposition rate. Preference tests indicated that tryptamine may act as an antiattractant or antifeedant in this species. The accumulation of the indole alkaloid tryptamine in plants may provide a mechanism for reducing insect reproduction, which is potentially useful in protecting crop plants.

Animals↗