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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↗

PubMed1999

Tryptamine-mediated stabilization of tryptophanyl-tRNA synthetase in human cervical carcinoma cell line.

Tryptamine is an endogenous neuroactive metabolite of tryptophan. Interpretation of the function of this bioamine, however, is restricted to manipulation with tryptamine synthetic pathways. Meanwhile, tryptamine is a potent inhibitor of protein biosynthesis, via the competitive inhibition of tryptophanyl-tRNA synthetase (TrpRS). The influence of the persistent tryptamine inhibition on the half-life and cellular content of TrpRS was examined by chase labeling of HeLa cells and the tryptamine-resistant subline with [35S]methionine. The results indicate that long-term tryptamine treatment of HeLa cells led to a significant increase in the half-life of TrpRS while the content, in vivo phosphorylation and gene dose of TrpRS were unchanged. These findings suggest that survival of drug-resistant cells may not be due to TrpRS gene amplification, but to stabilization of TrpRS. It was shown that tryptamine is an effective inhibitor of HeLa cell growth. In contrast to the well-characterized antineoplastic compounds, conferring a many hundred-fold elevated drug resistance to tumor cells, resistance to tryptamine at very low levels was difficult to achieve, i.e. the 2-fold resistant subline was selected after 19 months of treatment of HeLa cells with gradually increasing concentrations of tryptamine. The tryptamine-resistant HeLa subline exhibited a slower growth rate than the original HeLa line when similar concentrations of both cell populations were seeded on the plates. A low tryptamine resistance and a lack of TrpRS gene amplification were observed in two tryptamine-resistant HeLa sublines and three Chinese hamster sublines. The role of TrpRS in oncogenesis and the perspective for tryptamine as a potential anti-cancer drug are discussed.

Animals↗

PubMed1981

The effects of tryptamine on transmitter release at a lobster neuromuscular junction.

Electrophysiological techniques were employed to characterize the effects of tryptamine at excitatory and inhibitory neuromuscular junctions of the stretcher muscle in the carpopodite of lobster walking limbs. Tryptamine was found to have a concentration dependent, biphasic effect on excitatory junction potential (EJP) amplitude. At concentrations of 0.01-0.5 mM tryptamine increased the amplitude of evoked EJPs, but at higher concentrations (greater than 0.5 mM) the amplitude was decreased by this amine. The high concentrations also decreased the amplitude of inhibitory junction potentials (IJPs) and reduced the frequency of miniature excitatory junction potentials (MEJPs). When a preparation in which the EJPs had been depressed by tryptamine was washed with the control, artificial sea water solution, the EJPs were increased to an amplitude greater than that of the pre-tryptamine control. Current-voltage relationship studies showed that tryptamine did not affect the effective resistance of the muscle fiber membrane. Tryptamine had no effect on the amplitude of excitatory responses evoked by the iontophoretic application of glutamate. Concentrations of tryptamine ranging to 10.0 mM affected neither the conduction velocity in meropodite or that of giant central nervous system (CNS) axons. We conclude that tryptamine affects synaptic transmission pre-synaptically by influencing the transmitter release process. Mass spectrometric analysis showed tryptamine to be an endogenous substance in the lobster; but the concentrations were low in the tissues analyzed. The highest concentration (approximately 0.3 nmol/g wet tissue) was in the subesophageal ganglion. Tryptamine was not detected in the meropodite nerves or carpopodite muscles.

Animals↗

PubMed1981

In vivo pharmacological studies on the interactions between tryptamine and 5-hydroxytryptamine.

1 Three methods have been used in an attempt to study the interactions of tryptamine with central 5-hydroxytryptamine (5-HT) systems. 2 In grups of mice pretreated with tranylcypromine, tryptamine reduced the number of mice showing head twitches following the 5-HT precursor, 5-hydroxytryptophan. This effect was not seen in mice pretreated with saline and tryptamine itself did not induce head twitches in either group. 3 The swallowing reflex induced by 5-hydroxytryptophan in rats anaesthetized with urethane was substantially reduced by tryptamine injected into the internal carotid artery. This effect was seen in rats pretreated with saline or tranylcypromine, in the latter case the effects being more profound and longer lasting. In addition, swallowing evoked by the 5-HT uptake blocker, fluoxetine, and the 5-HT releaser, p-chloroamphetamine, was also reduced by tryptamine. 4 5-HT or noradrenaline injected intravenously into 5 day-old chicks caused a dose-dependent behavioural depression resembling sleep. Tryptamine at high doses caused behavioural alerting effects. Tryptamine at low doses had no overt effects but enhanced depression induced by 5-HT. At behaviourally excitatory doses tryptamine reduced the duration of the 5-HT depression. Noradrenaline-induced depression was not affected by high or low doses of tryptamine. 5 The results show that tryptamine can have complex actions on 5-HT systems depending on the parameter studied and support the notion that tryptamine may be a controlling factor in 5-HT-mediated transmission.

5-Hydroxytryptophan↗

PubMedDate not supplied

Motor response secondary to the release of endogenous serotonin by tryptamine in guinea-pig ileal longitudinal muscle with adherent myenteric plexus.

The mechanism of the contractile action of tryptamine on the longitudinal smooth muscle with adherent myenteric plexus in the guinea-pig ileum was reexamined in view of new evidence that tryptamine releases the enteric neural serotonin (5-HT) and noradrenaline. The desensitization to 5-HT abolished the contractile response to tryptamine (5 and 10 microM). The contractile response to tryptamine (1-5 microM) was progressively decreased by repeated application. The progressive decrease by tryptamine was more pronounced than that by exogenous 5-HT. Tetrodotoxin and atropine significantly decreased the contraction upon the 2nd trial of tryptamine (5 microM) by about 40% and 45% of the control, respectively. However, guanethidine or cocaine did not change the contraction by tryptamine (5 microM). A 5-HT uptake inhibitor, zimelidine, which had been demonstrated to block the release of preloaded [3H]5-HT by tryptamine (Takaki et al., 1985), intensively reduced the contractile response to tryptamine to the same extent as atropine. These results are consistent with the previous finding that tryptamine releases the physiologically active 5-HT from myenteric neurons (Takaki et al., 1985). The 5-HT released by tryptamine, at least in part, acts on myenteric cholinergic neurons, resulting in the muscular contraction.

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↗

PubMed1983

Hyperalgesia produced by the intrathecal administration of tryptamine to rats.

Tryptamine was applied directly into the spinal subarachnoid space of rats via permanently indwelling cannulas. Changes in pain-perception were measured by changes in the latency of the tail-flick in response to a radiant heat source of low intensity. While an intrathecal injection of serotonin has been previously shown to be analgesic, exogenous tryptamine produced dual effects on the pain-threshold, depending on the dose of tryptamine injected. Low doses of tryptamine (100 and 200 micrograms/rat) injected intrathecally onto the sacral area of the spinal cord appeared to be hyperalgesic by significantly decreasing the average tail-flick latency by 5 min after injection. Administration of the serotonin antagonist methysergide alone was without effect on the average tail-flick reaction time when injected either intrathecally or subcutaneously. However, pretreatment with either methysergide or cinanserin not only failed to inhibit tryptamine's potentiation of nociception, but actually enhanced the hyperalgesia produced by tryptamine. In contrast, a dose of 400 micrograms of tryptamine significantly increased the average tail-flick latency, suggesting an analgesic effect at this higher dose. This analgesic effect of 400 micrograms of tryptamine was completely inhibited by subcutaneously administered methysergide, while intrathecally injected methysergide produced even greater decreases in the tail-flick latencies after this high dose of tryptamine. These results suggest that tryptamine, although it differs from serotonin by only one hydroxyl group, may play a role in nociception which is opposite that played by serotonin.

Animals↗

PubMed1987

The behavioural effects of intravenously administered tryptamine in mice.

The behavioural effects of intravenously administered tryptamine were examined in mice. Tryptamine in a dose greater than 15 mg/kg induced distinct head-weaving and hindlimb abduction. These behavioural syndromes appeared immediately after the injection and disappeared within 3 min. The changes in time course of the behaviour induced by tryptamine were consistent with those of the levels of tryptamine in the brain. Pretreatment with p-chlorophenylalanine, a depleter of 5-hydroxytryptamine (5-HT), failed to alter the effects of tryptamine on head-weaving or hindlimb abduction but did result in head-twitches which were never seen after tryptamine alone. Metergoline strongly antagonized the behavior induced by tryptamine. Pirenperone and haloperidol inhibited the behavioural syndrome, antagonizing the head-weaving in particular. alpha-Methyl-p-tyrosine, a depleter of dopamine, reduced the head-weaving without affecting the hindlimb abduction. These results indicate that the 5-HT syndrome induced by intravenous administration of tryptamine is due to the direct effect of tryptamine on the 5-HT receptor. Tryptamine-induced behaviour, especially head-weaving, seems to be linked with dopaminergic neurones.

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↗

PubMed1986

Autoradiographic localization and pharmacology of unique [3H]tryptamine binding sites in rat brain.

The distribution and pharmacological specificity of [3H]tryptamine binding to coronal and horizontal sections of the rat brain were investigated with computer-assisted autoradiography. [3H]Tryptamine bound to brain regions with up to 58% specificity, as determined with 10 microM tryptamine as a displacer. The capacity (Bmax) of saturable [3H]tryptamine binding sites was greatest in the nucleus accumbens and claustrum (660-760 fmol mg protein-1), with intermediate binding site concentrations in hippocampus, septum, olfactory tubercle, frontal cortex, cingulate cortex and caudate-putamen. The phenylalkylamine, p-methoxyphenylpropylamine and the beta-carboline, harmaline, as well as 5-methyl-tryptamine, displaced [3H]tryptamine from each of these brain regions with a potency that approximated the 5-9 nM affinity (Kd) of [3H]tryptamine binding to each site. Only micromolar concentrations of serotonin displaced [3H]tryptamine, which did not bind to S1, S2, D1, D2 or alpha- or beta-adrenergic sites. The unique pharmacology and the regional overlap of [3H]tryptamine binding sites with dopaminergic nerve terminals in the nucleus accumbens and caudate-putamen suggest that tryptamine-containing neurons in the mammalian brain may modulate behavioral functions such as locomotion.

Animals↗

PubMed1993

Tryptamine: a metabolite of tryptophan implicated in various neuropsychiatric disorders.

Although early interest in the biomedical relevance of tryptamine has waned in recent years, it is clear from the above discussion that the study of tryptamine is worthy of serious consideration as a factor in neuropsychiatric disorders. The study of [3H]-tryptamine binding sites indicates an adaptive responsiveness characteristic of functional receptors. The question raised by Jones (1982d) on whether tryptamine is acting centrally as a neurotransmitter or a neuromodulator still remains mostly unanswered, although the evidence cited within this review strongly suggests a modulatory role for this neuroactive amine (see also Juorio and Paterson, 1990). The synthesis and degradative pathways of tryptamine, as well as the intricate neurochemical and behavioral consequences of altering these pathways, are now more fully understood. It is not yet clear what the role of tryptamine is under normal physiological [homeostatic] conditions, however, its role during pathological conditions such as mental and physical stress, hepatic dysfunction and other disorders of metabolism (i.e. electrolyte imbalance, increased precursor availability, enzyme induction or alterations in enzyme co-factor availability) may be quite subtle, perhaps accounting for various sequelae hitherto considered idiopathic. The evidence for a primary role for tryptamine in the etiology of mental or neurological diseases is still relatively poor, although the observations that endogenous concentrations of tryptamine are particularly susceptible to pharmacological as well as physiological manipulations serve to reinforce the proposition that this indoleamine is not simply a metabolic accident but rather a neuroactive compound in its own right. Finally, one might wonder what proportion of the data attributed to modifications of 5-HT metabolism might, in fact, involve unrecognized changes in the concentrations of other neuroactive metabolites of tryptophan such as tryptamine.

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↗

PubMed1987

Injections of deuterated tryptamine into the nucleus accumbens of the rat: effects on locomotor activity and monoamine metabolism.

Previous studies have shown that the systemic injection of tryptamine stimulates locomotion in rats and that the nucleus accumbens, a region involved in locomotion, contains the largest concentrations of binding sites for tryptamine in the brain of the rat. The present study examined the behavioral and neurochemical effects of bilateral injections into the accumbens of a deuterated analog of tryptamine, a,a-[2H]tryptamine. Injections of 25 micrograms a,a-[2H]tryptamine increased movements in rats at 25-70 min after injection and increased vertical (rearing) activity at 25-40 min. Injections of 50 micrograms of a,a-[2H]tryptamine produced a transient suppression of movement and vertical activity at 5-15 min, followed by increases in these activities at 40-65 min after injection that were comparable to the increases elicited by 10 micrograms of d-amphetamine. At 30 min after the injection of 50 micrograms a,a-[2H]tryptamine the concentration of dopamine in the nucleus accumbens was increased by 87%, and was preceded by a transient decrease in the level of the metabolite of dopamine homovanillic acid. The levels of 5-hydroxytryptamine and its major metabolite, 5-hydroxyindoleacetic acid in the nucleus accumbens were not changed. Thus, a,a-[2H]tryptamine may interact with tryptamine receptors in the nucleus accumbens to modulate locomotor behavior through mesolimbic dopamine neurons.

Animals↗

PubMed1994

The [3H]tryptamine receptor in human brain: kinetics, distribution, and pharmacologic profile.

The kinetics and distribution of [3H]tryptamine binding sites in human brain were investigated. Specific [3H]tryptamine binding in frontal cortex was of nanomolar affinity, reversible, saturable, and best fit to a single-site model. A heterogeneous distribution for this binding site was demonstrated, with the highest density observed in hippocampus, thalamus >> caudate nucleus, frontal cortex, pons, temporal cortex > globus pallidus/putamen, cerebellum. The similarities in kinetics and distribution of the [3H]tryptamine binding site in human and rat brain indicate that these two binding sites represent homologous structures. However, the present displacement studies using various ligands (indoleamines and other tryptophan metabolites, phenylethylamines, and miscellaneous drugs) and salts (Na+, K+, Ca2+, Mg2+, Cu2+) indicate stereospecific displacement as well as a rank-order potency profile that is different from that reported for the rat [3H]tryptamine binding site. This suggests the presence of distinct species-dependent [3H]tryptamine binding site subtypes. Taken together with the documented electrophysiological and behavioral evidence of tryptamine-mediated effects in the rat and the recent report of a significant loss of these binding sites in human portal systemic encephalopathy, as well as the present demonstration of an effect of guanine nucleotides on [3H]-tryptamine binding affinity, these findings suggest that these binding sites might be functional receptors. The implied role of tryptamine in neuropsychiatric disorders is supported by this demonstration of a receptor for [3H]-tryptamine in human brain.

Animals↗

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↗