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At least 19 recordsLinked to original sources
PubMed1990

Effects of protein-modifying reagents on brain tryptamine binding sites: possible involvement of a thiol group in temperature-induced high-affinity [3H]tryptamine binding sites.

To investigate the biochemical nature of temperature-induced high-affinity [3H]tryptamine binding sites, we subjected whole rat brain synaptic membranes to treatment with various protein-modifying reagents and examined the subsequent [3H]tryptamine binding properties of the membranes. Pretreatment of the membrane preparations with NEM, NBS, PCMB, PAPMA and MA, but not with iodoacetamide, DTT, glutathione and cysteine, reduced the [3H]tryptamine binding. In addition, to at least approx. 10(-4) M, the inactivation properties of NEM, PCMB, PAPMA and MA, except for NBS, were temperature-dependent. Furthermore, it was revealed that the Scatchard plot of [3H]tryptamine binding in membranes pretreated with these thiol reagents conformed to a curved line, as well as in the case of the control membranes. Nonlinear regression analysis of these data showed that NEM decreased the Bmax values of both the high and low affinity binding sites with no significant alteration in the KD values, whereas PCMB, PAPMA and MA increased only the KD value of the high affinity sites, accompanying the decrease of the Bmax values of both sites. These results indicate that the temperature-induced high-affinity [3H]tryptamine binding molecule(s) is a thiol protein.

Animals↗
PubMed1992

Application of tryptamine as a derivatizing agent for the determination of airborne isocyanates. Part 5. Investigation of tryptamine-coated XAD-2 personal sampler for airborne isocyanates in workplaces.

The development of an efficient solid sorbent personal sampler with increased convenience for sample collection in workplaces is described. Several solid sorbents were coated with tryptamine, and sampling tubes were prepared with the coated sorbents. These tubes were evaluated for the collection of phenyl isocyanate vapour generated in a commercial test atmosphere generation system that permits the simultaneous collection of up to 12 uniformly loaded samples. Tryptamine-coated XAD-2 resin was shown to be the most efficient solid sorbent for the collection of airborne phenyl isocyanate. The optimum amount of tryptamine needed for coating XAD-2 resin was investigated.

Air Pollutants, Occupational↗
PubMed1979

Relaxant response of goat trachea to 5-hydroxy-tryptamine mediated by D-tryptamine receptors.

1 Goat isolated trachea contracted in response to carbachol, histamine and 2-pyridylethylamine (an H(1)-receptor agonist) and relaxed after application of isoprenaline. 5-hydroxytryptamine (5-HT) and phenylephrine.2 Mepyramine, a selective H(1)-receptor antagonist, blocked histamine- and 2-pyridylethylamine-induced contractions. In high doses it also exhibited some nonspecific antagonism to carbachol. After H(1)-receptor blockade, 4-methylhistamine and dimaprit (specific H(2)-agonists) relaxed the carbachol-contracted trachea.3 Propranolol, a beta-adrenoceptor blocker, antagonized relaxation in response to isoprenaline and phenylephrine. In high doses, it produced a reversal of the phenylephrine response.4 Indomethacin enhanced contractions in response to carbachol and histamine.5 Relaxation to 5-HT was not affected by propranolol, indomethacin, metiamide or cimetidine (H(2)-blockers). These findings appear to exclude the involvement of adrenergic, prostaglandinergic and H(2)-histaminergic mechanisms in the mediation of this response.6 Atropine potentiated 5-HT-induced relaxations. This suggests the participation of a ;masked' excitatory cholinergic mechanism.7 Methysergide, dibenamine and dibenzyline selectively antagonized or reversed 5-HT-induced relaxation. Dibenamine and dibenzyline enhanced relaxations to isoprenaline.8 This investigation showed (i) a relaxant response of goat trachea to 5-HT, mediated via D-muscular tryptamine receptors; (ii) a small population of excitatory M-neuronal tryptamine and alpha-adrenoceptors; and (iii) predominance of H(1)-histamine receptors in the goat trachea.

Animals↗
PubMed1977

Selective introduction of TMS groups in tryptamines: preparation of N1-TMS derivatives of tryptamines.

Indolethylamines (tryptamines) with a primary animofunction react with Regisil under controlled conditions to yield a mono TMS derivative. Mass spectrometry to these derivatives shows that the TMS group is substituted on the indolic nitrogen (N1) and not the primary amino nitrogen. This is confirmed by converting these compounds to their isothiocyanate derivatives. The GC and GC-MS data of some typical compounds are presented.

Amino Acids↗
PubMed1985

Physiological responses of guinea-pig myenteric neurons secondary to the release of endogenous serotonin by tryptamine.

Intracellular recordings showed that administration of pulses of tryptamine mimicked one of the actions of serotonin (a slow depolarization associated with an increased input resistance) on type II/AH neurons of the myenteric plexus. After superfusion at high concentration tryptamine initially acted like serotonin, but then blocked the action of serotonin on these cells. Measurements of the release of preloaded [3H]serotonin or [3H]norepinephrine revealed that tryptamine is a potent releaser of these labeled amines; this release is Ca2+ independent but temperature dependent. Moreover, incubation with tryptamine depleted the myenteric plexus of endogenous serotonin. Since tryptamine has previously been demonstrated not to inhibit the binding of [3H]serotonin to its enteric neural receptor we framed the hypothesis that the serotonin-releasing action of tryptamine is responsible for its ability to mimic serotonin when given in pulses or to desensitize serotonin receptors through the prolonged release of serotonin when it is superfused. This hypothesis was tested by examining the action of tryptamine on the serotonin-mediated slow excitatory postsynaptic potentials evoked in type II/AH neurons by fiber tract stimulation. Tryptamine superfusion antagonized these slow potentials as predicted. Moreover, after a long time when endogenous serotonin was depleted, the response of type II/AH neurons to exogenous serotonin recovered but the slow synaptic potential did not. The action of tryptamine on this neuron was relatively specific. When the slow synaptic potential and serotonin responses were blocked by tryptamine the type II/AH neurons still responded to acetylcholine. Fast excitatory postsynaptic potentials were not affected by tryptamine. Furthermore, other types of neurons (I/S) and other neuronal responses to serotonin (such as a fast depolarization with decreased input resistance or presynaptic inhibition of acetylcholine release) were not blocked by tryptamine. Finally, radioautographic studies revealed a neural uptake of tryptamine in the chemically sympathectomized myenteric plexus; however, the distribution of tryptamine in the plexus was different from that of serotonin and was not blocked by excess non-radioactive serotonin. Therefore tryptamine does not enter myenteric neurons via the specific serotonin uptake mechanism; however, zimelidine, found to be a selective inhibitor of the enteric uptake of serotonin, antagonized the release of serotonin by tryptamine and attenuated the effect of tryptamine on responses to serotonin.(ABSTRACT TRUNCATED AT 400 WORDS)

5-Methoxytryptamine↗
PubMed1988

Effects of tryptamine mediated through 2 states of the 5-HT2 receptor in calf coronary artery.

The mode of action of tryptamine was investigated on strips of left circumflex coronary artery of calf. 1) Exposure to (-)-deprenyl, an irreversible inhibitor of monoamine oxidase B, markedly potentiated the contractions caused by tryptamine but not those by 5-hydroxy-tryptamine (5-HT). Experiments were therefore carried out on arteries treated with (-)-deprenyl. 2) Tryptamine, administered non-cumulatively, elicited fast developing contractions, which partially faded. The intrinsic activity for the peak response to tryptamine was 0.8 compared to 5-HT. Ketanserin competitively antagonized the tryptamine-induced contractions with a KB of (-log mol/l) 9.9. Methysergide antagonized the effects of tryptamine in a noncompetitive manner by depressing the maximum response with an IC50 (-log mol/l) greater than 9.0. 3) Tryptamine caused unsurmountable depression of 5-HT-induced contractions with an IC50 (-log mol/l) of 6.4. Ketanserin also competitively antagonized the depressant effects of tryptamine on 5-HT-induced contractions with a KB of (-log mol/l) 9.9. 4) At high concentrations of tryptamine (0.2-1 mmol/l), the fast developing contractions were followed by slowly developing contractions. Methysergide 1 nmol/l enhanced maximally the slow developing contractions. 5) These findings are consistent with an interaction of tryptamine at different sites of the allosteric 5-HT2-receptor system: (I) Tryptamine competes with ketanserin for the 5-HT2-receptor in the highly active R state. Binding of tryptamine to the R state would cause the fast contraction. (II) Tryptamine competes with ketanserin for the allosteric sites.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

The modulatory effects of tryptamine and tyramine on the S9-mediated mutagenesis of IQ and MeIQ in Salmonella strain TA98.

The S9-mediated mutagenesis of IQ and MeIQ in Salmonella strain TA98 was modulated by introduction to the assay of tryptamine or tyramine. Both biogenic amines inhibited or enhanced the mutagenic response as a function of amine concentration, strain of rat used as the S9 source, and the IQ-type mutagen tested. Enhancement of IQ mutagenesis by tryptamine (10-80 microM) was observed in the presence of S9 preparations derived from Aroclor 1254-pretreated Fischer rats; the enhancing effect ceased at tryptamine concentrations > 160 microM. When Sprague-Dawley-S9 or Wistar-S9 were used for activation, the enhancement of IQ mutagenesis by tryptamine shifted to inhibition at tryptamine concentrations > 40 microM, with Sprague-Dawley-S9, and > 20 microM, with Wistar-S9. By contrast, MeIQ-mutagenesis was enhanced by tryptamine (10-160 microM), regardless of the rat strain used as S9 source. Tyramine was a weaker enhancer of MeIQ mutagenesis than was tryptamine and, unlike tryptamine, its inhibitory effects on IQ mutagenesis were observed only with Wistar-S9. Tryptamine (10-80 microM) inhibited cytochromes P450IA1 and P450IA2 activities, monitored by the O-deethylation of ethoxyresorufin and Glu-P-1 mutagenesis in TA98, respectively. These data suggest that the effects of biogenic amines on IQ and MeIQ bioactivation are complex. Furthermore, this study demonstrates that tryptamine and tyramine act both as enhancers (comutagens) and as inhibitors (antimutagens) of IQ and MeIQ mutagenesis, depending on the testing conditions.

Animals↗
PubMed1989

A comparison of the effects of tryptamine and 5-hydroxytryptamine on feeding following injection into the paraventricular nucleus of the hypothalamus.

The effects of 5-hydroxytryptamine (5-HT) and tryptamine injected into the paraventricular nucleus of the hypothalamus (PVN) on food intake, and on noradrenaline- (NA) induced feeding were examined. In nondeprived rats, 12.5-100 nmol 5-HT reduced the intake of palatable wet mash diet over a 30-minute period. Tryptamine (50 and 100 nmol) was without effect in this paradigm. However, when tryptamine was injected into the PVN of rats pretreated with the monoamine oxidase inhibitor, pargyline, a strong anorectic effect was observed. The action of tryptamine in pargyline-treated rats was not affected by depletion of 5-HT levels in the PVN with PCPA. This indicates that the effect of tryptamine is not mediated by a release of endogenous 5-HT. Tryptamine injected into the PVN potentiated the effect of a low dose of 5-HT on food intake. This effect may be due to a prolongation of the activity of 5-HT resulting from tryptamine competing with 5-HT for the same reuptake system. Tryptamine and 5-HT attenuated the feeding response elicited by injection of 25 nmol NA into the PVN. Both tryptamine and 5-HT were more potent at attenuating the effects of NA than in reducing the intake of the palatable wet mash diet. Overall, the results suggest that tryptamine may act via the serotonergic system in the PVN to affect food intake, but it is a weaker compound than 5-HT in this respect.

Animals↗
PubMed1978

Effects of tryptamine on active sodium and chloride transport in the isolated bullfrog cornea.

The effects of the serotonin analogue, tryptamine, on the active transepithelial transport of Na+ and Cl- in the in vitro bullfrog cornea were studied. Tryptamine, 1 mM, inhibited both the short-circuit current (Isc) and potential difference (PD) of corneas transporting either Na+ alone or both Na+ and Cl-. The electrical resistance, R, increased in all cases. Both unidirectional Na+ and Cl- fluxes were decreased by tryptamine and these changes accounted for the inhibitory effects on the Isc. The effects of tryptamine were considered along with those of 2 mM theophylline and 0.1 mM ouabain. Tryptamine inhibited the Isc and both undirectional Cl- fluxes which were previously stimulated by theophylline. Theophyline addition, after tryptamine preincubation, increases the Cl- undirectional fluxes but did not restore the inhibited Isc. The inhibitory effects of tryptamine on active Na+ and Cl- transport were different from those of ouabain. While both drugs inhibited the forward Na+ and Cl- fluxes, their backfluxes decreased with tryptamine and increased with ouabain. The addition to the bathing solution of tryptamine after ouabain preincubation reduced the ouabain-increased backward Cl- flux and further increased the electrical resistance. These results are analyzed in terms of an electrical model from which it appears that trypamine's mechanism of action was to decrease cellular permeability to the transepithelial movement of Na+ and Cl-.

Animals↗
PubMed1989

Tryptamine receptors: neurochemical and electrophysiological evidence for postsynaptic and functional binding sites.

[3H]Tryptamine binding characteristics and responsiveness of spontaneously active caudate nucleus neurons to intravenous application of drugs were assessed 6 weeks following unilateral application of 6-hydroxydopamine (6-OHDA, 8 micrograms) to the substantia nigra of male Wistar rats. The effects of this lesion procedure on caudatal levels of dopamine, 5-hydroxytryptamine (5-HT) and their acid metabolites, and on pargyline-induced (200 mg/kg, 2 h, s.c.) accumulation of tryptamine in the caudate nucleus were also assessed. Levels of caudatal dopamine and metabolites were reduced ipsilateral to the lesion. Concurrently there was a reduction in the extent of pargyline-induced tryptamine accumulation. Caudatal [3H]tryptamine binding was increased ipsilateral to the lesion, indicating a postsynaptic localization of this binding site. Bmax values in the caudatal samples ipsilateral to the lesion were increased by an average of 34% relative to the contralateral side. Contralateral Bmax values were equivalent to those routinely obtained in control animals. The affinity (Kd) of these binding sites for [3H]tryptamine was unchanged by the lesion procedure. The firing rate of caudate neurons was inhibited by intravenous application of tryptamine, apomorphine and 5-MeODMT. The lesion procedure did not affect these responses to 5-MeODMT. Responses to tryptamine and to apomorphine were enhanced ipsilateral to the lesion by 10- and 3-fold respectively. Haloperidol (0.5 mg/kg, i.v.) reversed apomorphine-induced inhibition of caudatal neuronal firing rate. The effects of tryptamine were not reversed by haloperidol. These data indicate a classical adaptive increase in [3H]tryptamine binding in caudate following 6-OHDA lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1985

Tryptamine concentrations in areas of 5-hydroxytryptamine terminal innervation after electrolytic lesions of midbrain raphe nuclei.

The possible existence of tryptamine-containing neurons originating in the midbrain raphe is suggested by several reports of tryptamine-mediated responses to electrical stimulation of the raphe nuclei. To assess this hypothesis, we have investigated the effects of electrolytic lesions of the median and dorsal raphe nuclei on striatal, hypothalamic, and hippocampal concentrations of tryptamine, 5-hydroxytryptamine (5-HT), and 5-hydroxyindoleacetic acid. In addition, the rat striatal tryptophan concentrations were also determined. No changes in the concentrations of tryptamine were observed at 1 or 2 weeks after lesioning the dorsal and median raphe nuclei, at which time the other 5-hydroxyindoles were markedly reduced; furthermore, no reductions were observed in tryptamine concentrations in the striatum, hypothalamus, or hippocampus of rats pretreated with a monoamine oxidase inhibitor. The only change observed in these rats was a limited increase in striatal tryptamine and tryptophan observed at 1 day after lesioning. The results indicate that tryptamine concentration is independent of the integrity of 5-HT-containing neurons of the midbrain raphe nuclei. Furthermore, if tryptamine-containing neurons that have terminal projections to the striatum, hypothalamus, and hippocampus exist, their cell bodies are located in regions outside the dorsal and median raphe nuclei. Another possibility could be that tryptamine is located in glial cells.

Animals↗
PubMed1985

Tryptamine-induced vasoconstrictor responses in rat caudal arteries are mediated predominantly via 5-hydroxytryptamine receptors.

It has been suggested that tryptamine can stimulate specific receptors distinct from those for 5-hydroxytryptamine (5-HT). We have examined this possibility in the rat isolated caudal artery, paying particular attention to the involvement of monoamine oxidase metabolism and alpha-adrenoceptors, two factors that can complicate the quantification of antagonist potencies at 5-HT receptors. 5-HT and tryptamine were agonists over the concentration-ranges 3.0 X 10(-8) - 3.0 X 10(-5) mol l-1 and 1.0 X 10(-6) - 3.0 X 10(-4) mol l-1 respectively. The sensitivity of the caudal artery to tryptamine was increased by about 44 fold in the presence of iproniazid (5.0 X 10(-5) mol l-1) and about 17 fold in the presence of pargyline (1.0 X 10(-5) mol l-1), while responses to 5-HT and methoxamine were unaffected. In the absence of iproniazid, ketanserin and methysergide were potent antagonists of responses to 5-HT with pA2 values of 9.08 and 9.11 and slopes of the Schild regressions of 1.15 and 1.00 respectively. However, against tryptamine the antagonists were weaker such that pA2 values were similar to those against 5-HT but the slopes of the Schild regressions were 0.47 and 0.47. In the presence of iproniazid (or pargyline), the 5-HT antagonists were more potent against tryptamine such that the pA2 values and the slopes of the Schild regressions were not significantly different from those against 5-HT. Phentolamine was a weak antagonist of responses to both 5-HT and tryptamine in the presence of iproniazid. 5 The findings in this study suggest that the contractile action of tryptamine in rat caudal artery is mediated predominantly by the same receptor as 5-HT and that the differential inactivation of tryptamine by monoamine oxidase enzymes largely accounts for the different susceptibilities of 5-HT and tryptamine to the antagonists examined.

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↗
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↗
PubMed1988

[3H]tryptamine binding sites are not identical to monoamine oxidase in rat brain.

Competition binding studies, subcellular distribution, and in vitro autoradiography were employed to compare the binding in rat brain of [3H]tryptamine with two radioligands for monoamine oxidase (MAO), [3H]pargyline, and [3H]1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine ([3H]MPTP). The MAO inhibitors pargyline, clorgyline, and deprenyl all yielded biphasic competition curves versus [3H]tryptamine. At low concentrations, these drugs stimulated binding by protecting the radioligand from MAO oxidation; at considerably higher concentrations, they inhibited binding by direct competition at the [3H]tryptamine binding site. In subcellular distribution studies, [3H]tryptamine was localized preferentially to the synaptosomal fraction, whereas [3H]pargyline showed greater binding to the mitochondrial fraction. Equilibrium binding studies revealed that the potencies of a series of seven compounds at inhibiting [3H]tryptamine binding were completely different from their potencies at inhibiting [3H]MPTP binding. Finally, the autoradiographic distribution of [3H]tryptamine binding in rat brain was different from that of [3H]MPTP and [3H]pargyline. We conclude that the [3H]tryptamine binding site in rat brain is not equivalent to MAO.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1978

Tryptamine-induced drug effects insensitive to serotoninergic antagonists: evidence of specific tryptaminergic receptor stimulation?

The drug effects of tryptamine and 5-hydroxytryptopham (5-HTP) in the rabbit were compared following monoamine oxidase inhibition and various drug pretreatments. Both agents evoked hyperthermia and behavioural excitation; tryptamine but not 5-HTP also produced forepaw clonic activity. Serotoninergic receptor blockers abolished the effects of 5-HTP but only weakly influenced tryptamine responses. Both tryptamine and 5-HTP effects were potentiated by fluoxetine. Methergoline, a putative tryptaminergic receptor blocker, antagonized tryptamine-induced hyperthermia and forepaw clonus but did not influence 5-HTP responses. It is postulated that while 5-HTP produces its effects through a serotoninergic mechanism, some of the responses to tryptamine result from activation of a specific tryptamine-sensitive mechanism.

5-Hydroxytryptophan↗
PubMed1985

Analysis of the cardiovascular responses to central injection of tryptamine in rats.

Tryptamine (2-20 micrograms), administered into the lateral cerebral ventricle of the rat, evoked a pressor response which was sometimes followed by a prolonged depressor response. The intracisternal administration of tryptamine (7-20 micrograms) caused a slow progressive and long-lasting depressor effect without or with an initial pressor effect. The pressor response was accompanied by variable changes in heart rate, whilst the pure depressor response was accompanied by a decrease in heart rate. After transection of the spinal cord between C1 and C2 the pressor response was substantially reduced or abolished. Methysergide, injected centrally, antagonized in a dose-dependent manner the pressor effect, whilst p-chlorophenylalanine, atropine and hexamethonium, administered by the same route, did not diminish this effect. It is concluded that tryptamine, injected centrally, causes both increases and decreases in arterial blood pressure and heart rate. The pressor response to tryptamine results from the activation of central noncholinergic, methysergide-sensitive, receptor sites and the depressor response to tryptamine may be due to a centrally-induced reduction in sympathetic nervous activity. It is tentatively suggested that tryptamine, like 5-hydroxytryptamine, participates in the physiological regulation of the cardiovascular system of the rat, as both a central excitatory and inhibitory regulator.

Animals↗