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PubMed1981

Comparison of the cardiovascular responses to intracerebroventricular administration of tryptamine, 5-hydroxytryptamine, tryptophan and 5-hydroxytryptophan in rats.

General characteristics of the cardiovascular responses to intracerebroventricular (i.c.v.) injection of tryptamine, 5-hydroxytryptamine (5-HT), tryptophan and 5-hydroxytryptophan (5-HTP) were compared. Relatively small doses of tryptamine and 5-HT (0.005-0.1 microM) produced considerable, long-lasting and dose-dependent pressor effects, which sometimes were followed by prolonged depressor effects. Tryptophan (0.02-0.5 microM) and 5-HTP (0.02-0.2 microM) caused variable and usually slight, but long-lasting, vascular responses or no vascular response A large dose of tryptamine (0.5 microM) evoked variable vascular effects, while the same dose of 5-HT and 5-HTP evoked marked and prolonged depressor effects. The vascular responses to the drugs were accompanied by variable changes in heart rate. Tryptamine, 5-HT and 5-HTP, in the majority of rats, produced a bradycardia. The present study provides evidence that the cardiovascular response to i.c.v. administration of tryptamine is similar to that of 5-HT, supporting the idea that tryptamine, in addition to 5-HT, participates in the central physiological regulation of the rat cardiovascular system. The role of tryptophan and 5-HTP by themselves in this regulation, if any is of secondary importance.

5-Hydroxytryptophan↗
PubMed1976

Actions of methoxamine and tryptamine and their interactions with cyproheptadine and phenoxybenzamine on cat spinal cord segmental reflexes.

The effects of norepinephrine, methoxamine and tryptamine were assessed on the monosynaptic and polysynaptic segmental reflexes in the unanesthetized, decerebrated acute spinal cat. Their selectivity of action was determined by studying the interactions of methoxamine and tryptamine with two antagonists, cyproheptadine and phenoxybenzamine. Potentials were evoked by stimulating either the L7 or S1 dorsal root and were recorded from the corresponding ipsilateral ventral root. Norepinephrine did not affect reflex activity, whereas methoxamine facilitated both the monosynaptic and polysynaptic potentials in a dose-related manner when infused over 20 minutes. Tryptamine facilitated both the monosynaptic and polysynaptic reflex potentials. This increase was dose related for the monosynaptic reflex but not for the polysynaptic reflex. Phenoxybenzamine blocked the facilitatory effects of methoxamine and did not antagonize the effects of tryptamine on the segmental reflex. The facilitatory effects of tryptamine were effectively blocked by cyproheptadine. Cyproheptadine failed to reduce the polysynaptic response to methoxamine, although it partially antagonized the monosynaptic facilitation. These findings demonstrate that methoxamine and tryptamine facilitate the segmental reflex by different modes of action and provide additional evidence for noradrenergic and tryptaminergic systems in the spinal cord.

Animals↗
PubMed1986

5-HT-mediated myoclonus in the guinea pig as a model of brainstem 5-HT and tryptamine receptor action.

Indoleamine-induced myoclonus in guinea pigs is a specific model of brainstem 5-HT function that can be used to characterize the indoleamine systems initiating myoclonus. 5-HT precursors and indole-containing 5-HT agonists induce myoclonus in guinea pigs, but piperazine-containing compounds do not. This selectivity of action correlates with the ability of 5-HT agonists to act at 5-HT-1 receptors. Further evidence for the involvement of a brainstem 5-HT receptor subpopulation in the initiation of myoclonus is shown by the differential ability of 5-HT antagonists to inhibit 5-HTP-induced myoclonus and of 5-HT reuptake blockers to potentiate threshold myoclonus. Distinct tryptamine receptors also may be involved in producing myoclonus, since indoleamine antagonists show differing potencies in inhibiting 5-HTP- and tryptamine-induced myoclonus. Tryptamine-induced myoclonus is, however, dependent on intact presynaptic 5-HT function. Biochemical studies indicate that 5-HT is primarily responsible for 5-HTP-evoked myoclonus, whereas tryptamine predominates in tryptamine-induced myoclonus. Both 5-HT and tryptamine may contribute to myoclonus produced by L-tryptophan. Indoleamine-induced myoclonus in guinea pigs may be valuable in studying the organization of brainstem indoleamine systems that may be involved in some forms of human myoclonus.

5-Hydroxytryptophan↗
PubMed1989

Biochemical characterization of [3H]tryptamine binding sites from rat brain.

Rat brain membranes were treated with different protein modifying reagents, all of which were able to reduce [3H]tryptamine binding. However, inactivation by N-ethylmaleimide and iodoacetamide only was counteracted by coincubation with tryptamine. Thus, the [3H]tryptamine binding molecule is a membrane protein with an essential sulfhydryl group at the binding site. After incubation of digitonin-solubilized membranes with seven different lectins, no precipitation of [3H]tryptamine binding sites was observed. On concanavalin A and wheat germ agglutinin affinity chromatography, no [3H]tryptamine binding activity was found to be specifically bound. Therefore, the [3H]tryptamine binding protein appears to be devoid of lectin binding carbohydrate residues.

Animals↗
PubMed1986

[3H]tryptamine autoradiography in rat brain and choroid plexus reveals two distinct sites.

In vitro autoradiographic techniques were used to examine the distribution of [3H]tryptamine binding sites in rat brain. The gross distribution and pharmacological characteristics of binding to brain sections resembled those seen in homogenate studies. Binding sites were found throughout the brain, with a preponderance of sites in the forebrain and limbic structures; highest levels were seen in the choroid plexus and the interpeduncular nucleus. Other regions exhibiting high levels of [3H]tryptamine binding include the cortex (especially lamina I), caudate putamen, hippocampus, anterior olfactory nucleus, olfactory tubercle, nucleus accumbens, amygdala, superior colliculus (superficial gray layer), locus ceruleus, the nucleus of the solitary tract and the pineal body. Although there were similarities in this distribution to that for binding sites of [3H]5-hydroxytryptamine ([3H]serotonin), the overall patterns were distinct. The binding site for [3H] tryptamine in the choroid plexus (termed T-2) was pharmacologically distinct from that in the rest of the brain (termed T-1); several compounds, including kynuramine, were potent inhibitors of [3H]tryptamine binding at the brain site, but not at the choroid plexus site. [3H]Serotonin also labels a site in the rat choroid plexus; this site was different from both [3H]tryptamine sites. Knowledge of the distribution of tryptamine binding sites in the brain will aid in efforts to ascertain the function of these sites.

Animals↗
PubMed1986

Autoradiographic localization of tryptamine binding sites in the rat and dog central nervous system.

Tryptamine, an endogenous trace amine, is currently postulated to be a neuromodulator or neurotransmitter in the mammalian CNS. High-affinity binding sites have been described for tryptamine in rat brain homogenate preparations. The present study further characterizes tryptamine binding throughout the CNS and delineates its distribution using in vitro receptor binding in conjunction with autoradiographic techniques. Saturation studies on 20-micron-thick brain sections suggest a single class of binding sites (Hill coefficient = 0.97 +/- 0.04) with a high affinity (KD = 4.79 +/- 1.55 nM). In competition studies, kynuramine and tetrahydrobetacarboline significantly inhibited H3-tryptamine binding while serotonin, dopamine, and phenylethylamine failed to significantly inhibit it. The most potent inhibitor of H3-tryptamine binding was tryptamine (KI = 4.19 +/- 2.13 nM). In rat brain sections processed for in vitro autoradiography, highest binding occurred in the following limbic structures: the accumbens nucleus, the amygdalohippocampal area, the lateral septal nucleus, the entorhinal cortex, and the anterior olfactory nucleus. At diencephalic levels, the highest binding was observed in the reuniens thalamic nucleus, the paraventricular thalamic nucleus, the medial habenular nucleus, the central medial thalamic nucleus, and the arcuate hypothalamic nucleus. In the midbrain of the rat, binding was most notable in the interpeduncular nucleus, the superficial layer of the superior colliculus, the periaqueductal gray, and the paranigral nucleus. In the lower brain stem of the dog, binding was evident in the external cuneate nucleus, the spinal trigeminal nucleus, and in the region of the solitary nucleus. Binding was also present in both the ventral and dorsal horns of the canine spinal cord.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1979

The influx of tryptamine into snail (Helix pomatia) ganglia: comparison with 5-hydroxytryptamine.

Isolated ganglia possess the ability to concentrate tryptamine from an external medium by a process which is temperature sensitive and independent of sodium and other cations. Kinetic analysis of the accumulation process showed the influx of tryptamine to be a single mechanism with Km and Vmax values of 1.4 X 10(-4)M and 5 X 10(-8) mole/g/min. The influx of tryptamine is an unspecific process and is insensitive to a number of metabolic inhibitors and various analogues. The process of tryptamine influx is thus similar in principle to the low affinity uptake mechanism for 5-HT (see Osborne et al., 1975). The present data, which include some experiments on the release of 5-HT and tryptamine, are discussed from the point of view of a functional role for 5-HT and tryptamine in the snail CNS.

Adenosine Triphosphate↗
PubMed1998

Modulation of CYP1A2 enzyme activity by indoleamines: inhibition by serotonin and tryptamine.

Recent evidence supports a role for the CYP2D6 enzyme in the metabolism of tryptamine. Because of the partial overlapping between substrate and inhibitor specificities that characterize some cytochrome P450 enzymes, these finding raise the possibility that other cytochrome P450 enzymes may be modulated by endogenous compounds. In the present study, the occurrence of modulatory effect of 17 neurotransmitters, precursors and metabolites on the cytochrome P450 1A2 (CYP1A2) enzyme activity was studied in human liver microsomes. Two indoleamines, serotonin and tryptamine, showed a competitive inhibitory effect on the high-affinity component of the phenacetin O-de-ethylase activity. Both substances induced an inhibition of 100% of the activity, with Ki values of 35 and 45 microns for serotonin and tryptamine, respectively. The inhibitors did not affect the microsomal NADPH-reductase activity. Other substances, which were either poor or partial inhibitors, were dopamine, L-tyrosine, tryptophol, 5-hydroxytryptophol, adrenaline, indole-3-acetaldehyde, 5-hydroxytryptophan, noradrenaline, vanillylmandelic acid, indole-3-acetic acid, dihydroxyphenylacetic acid, and homovanillic acid. L-tryptophan, dihydroxyphenylalanine and 5-hyroxyindole acetic acid induced very low or no inhibitory effect. Tryptamine and serotonin metabolism in human liver microsomes was studied after inhibition of monoamine oxidase activity with the unspecific MAO inhibitor pargyline. Both serotonin and tryptamine were metabolized in human liver microsomes. However, the metabolism of both indoleamines was not significantly inhibited with the CYP1A2-specific inhibitor furafylline, thus indicating that the inhibition of CYP1A2 was not related to metabolic activity of the CYP1A2 enzyme on serotonin or tryptamine. The CYP1A2 enzyme is expressed in brain and is involved in the metabolism of psychoactive drugs. Therefore, the fact that endogenous compounds could modulate the CYP1A2 activity suggests that local activity of brain CYP1A2 might be susceptible to local regulatory mechanisms. This may have important clinical implications, one of them being that CYP1A2 activity in brain tissue might correlate poorly with that of liver, as observed in vivo. In addition, the influence of indoleamines on CYP1A2 activity might be partly responsible for a number of associations of CYP1A2 activity with nutritional and environmental factors.

Brain↗
PubMed1998

Stark Spectroscopy of Tryptamine Immobilized on a Gold Electrode.

Electroreflectance (ER), ellipsometry, and surface-enhanced Raman spectroscopy (SERS) measurements were performed for immobilized tryptamine on polycrystalline gold electrodes. SERS study indicates that the indole ring does not interact directly with the gold surface. Ellipsometric measurements yielded a thickness of the tryptamine layer of (1.98 +/- 0.05) nm and an inferred surface concentration of 3.3 x 10(-6) mol/m2. ER measurements were performed in the wavelength region 200-300 nm using the NIST synchrotron ultraviolet radiation facility (SURF). The ER response was interpreted as a Stark shift in the tryptamine absorption line at 218 nm. Assuming that the tryptamine layer consists of two stacked tryptamine molecules associated at the indole rings, a unified analysis of ER and ellipsometric data gave the difference between the static dipole moments of the solvated ground and excited states of 0.65 x 10(-30) C m in low ionic strength buffer (0.01 M PBS) and 0.25 x 10(-30) C m in high ionic strength buffer (0.01 M PBS + 1.0 M NaClO4). The results point to the importance of the composition of the solvation shell. Semiempirical quantum chemistry calculations of tryptamine molecules gave a qualitative explanation of the ER response in the low ionic buffer. The large ER response suggests that the method could be applied to the study of the tryptophan environment in adsorbed proteins. Copyright 1998 Academic Press.

Journal Article↗
PubMed1959

The relative activities of some tryptamine analogues on the isolated rat stomach strip preparation.

The relative potencies of analogues of tryptamine and 5-hydroxytryptamine have been determined on the rat fundus preparation. This tissue had an amine oxidase activity, which, in the homogenate, was able to inactivate both tryptamine and 5-hydroxytryptamine to about the same degree. Amine oxidase inhibitors potentiated the action of tryptamine and many analogues on the isolated rat fundus preparation, but not the action of 5-hydroxytryptamine or of other hydroxytryptamines. This suggested that, in the isolated organ, the amine oxidase was unable to inactivate 5-hydroxytryptamine, but could inactivate tryptamine, 5-methoxytryptamine and many others. These results may be explained if it is supposed that tryptamine entered the cell, but because of the polar hydroxyl group 5-hydroxytryptamine did not. This hypothesis is supported by the oil/water partition coefficients. The structure/activity of the various tryptamine derivatives is discussed in the light of this assumption.

5-Methoxytryptamine↗
PubMed1989

Down-regulation of tryptamine binding sites following chronic molindone administration. A comparison with responses of dopamine and 5-hydroxytryptamine receptors.

The present study assessed changes of tryptamine, dopamine D2, 5-HT1 and 5-HT2 binding sites in rat brain following chronic treatment with low (5 mg/kg/day) and high (40 mg/kg/day) doses of molindone, a clinically effective psychotropic drug. The high-dose molindone treatment produced a decrease in the number of tryptamine binding sites while both high and low doses caused an increase in the number of dopamine D2 binding sites in the striatum. No significant changes were observed in either 5-HT1 or 5-HT2 binding sites in the cerebral cortex. Competition binding experiments showed that molindone was a potent inhibitor at dopamine D2 but less effective at tryptamine, 5-HT1 and 5-HT2 binding sites. The inhibition activity of molindone towards type A monoamine oxidase produced a significant increase in endogenous tryptamine accumulation rate which was much higher than that of dopamine and 5-HT. These findings suggest that the reduction in the number of tryptamine binding sites produced by chronic molindone administration is related to monoamine oxidase inhibition and that the increase in the number of dopamine D2 binding sites is correlated to receptor blocking activity of the drug.

Animals↗
PubMed1978

LSD and tryptamine effects on sleep/wakefulness and electrocorticogram patterns in intact cats.

Effects of intravenous infusions of LSD (3.75, 7.5, 15 microgram/kg over 5 min; crossover N = 4) and tryptamine (0.04, 0.08, 0.12 mg/kg/min for 150 min; crossover N = 6) were compared to saline in intact cats through observation of five sleep/waking patterns. Electrocorticogram (ECoG) was analyzed for frequency band indices and mean amplitude and frequency. LSD increases wakefulness and drowsiness and decreases spindle sleep and rapid eye movement (REM) sleep during the first 75 min (period 1). The increase in active wakefulness and decrease in REM sleep persist during period 2, with an increase in spindle sleep thereafter. LSD increases delta index and ECoG amplitude, with a decrease in ECoG frequency; these effects peaked in period 2. Tryptamine increases wakefulness and drowsiness during period 1, with decreases in spindle sleep and REM sleep. The increase in quiet wakefulness and decrease in REM sleep persist during period 2, but no significant tryptamine effect is seen in sleep/waking patterns after infusion ceases. ECoG frequency increases during tryptamine infusion (periods 1 and 2), while ECoG amplitude increases during periods 2 and 3. Thus LSD and tryptamine both increase wakefulness, decrease spindle sleep, and decrease REM sleep.

Animals↗
PubMed1977

Responses of the flexor reflex to LSD, tryptamine, 5-hydroxytryptophan, methoxamine, and d-amphetamine in acute and chronic spinal rats.

The flexor reflex of acute (40-48 h after mid-thoracic spinal transection) and chronic (at least 2 months after transection) spinal rats was evoked by tetanic electrical stimulation of both hindfeet and recorded on a polygraph using a transducer connected to the left hindfoot. The flexor reflex in the chronic spinal rat was more responsive to electrical stimulation and to the actions of drugs studied than was the flexor reflex in the acute spinal rat. In chronic spinal rats, d-amphetamine, methoxamine, LSD, tryptamine, and 5-hydroxytryptophan (5-HTP) facilitated the flexor reflex and induced spontaneous movements. These facilitative effects were seen in acute spinal rats only when much larger i.p. doses of amphetamine, methoxamine, and LSD were used. Small i.v. doses of tryptamine also produced the facilitation. The facilitation caused by LSD and tryptamine, but not 5-HTP, in chronic spinal rats was antagonized by cyproheptadine. These observations suggest that chronic spinal rats were more sensitive to the drugs than acute spinal rats and support the hypothesis that the mode of action of LSD is similar to that of tryptamine but different from that of 5-HTP since cyproheptadine antagonized the facilitative effects of LSD and tryptamine but not those of 5-HTP.

5-Hydroxytryptophan↗
PubMed1993

Effects of age and of chronic antidepressant treatment on [3H]tryptamine and [3H]dihydroalprenolol binding to rat cortical membranes.

1. The effects of age and of chronic antidepressant treatment on [3H]tryptamine and [3H]dihydroalprenolol binding site density were measured in brain cortical membranes from male Sprague-Dawley rats. 2. The density but not the affinity of [3H]tryptamine binding sites was increased in 18-month-old rats relative to 3-month-old rats. Neither the density nor the affinity of [3H]dihydroalprenolol binding sites was affected by age. 3. Chronic administration (28 days s.c. via Alzet osmotic minipumps) of tricyclic antidepressant drugs (daily doses: imipramine.HCl, 30 mg kg-1; desipramine.HCl, 10 mg kg-1; clomipramine.HCl, 10 mg kg-1) resulted in decreases in [3H]dihydroalprenolol binding site density but no changes in [3H]tryptamine binding site density; no changes in affinity of either site were observed. 4. Chronic administration (s.c. via Alzet osmotic minipumps) of monoamine oxidase inhibitor antidepressant drugs (daily doses: tranylcypromine.HCl, 0.5 and 1.0 mg kg-1; phenelzine sulfate, 5 and 10 mg kg-1, each for 28 days; clorgyline.HCl, 1.0 mg kg-1; (-)-deprenyl.HCl, 1.0 mg kg-1, each for 14 days) resulted in decreases in [3H]tryptamine binding site density, without any effects on the affinity of this site. In addition, each of these monoamine oxidase inhibitors except (-)-deprenyl resulted in a decrease in [3H]dihydroalprenolol binding site density. No affinity changes were observed. 5. These data indicate that the [3H]tryptamine binding site exhibits physiological changes with aging and is differentially sensitive to the actions of tricyclic antidepressants and monoamine oxidase inhibitor antidepressants, respectively.

Age Factors↗
PubMed1994

Effects of tryptamine on plasma glucagon levels in mice.

Our previous study indicated that tryptamine induces a dose-related increase in plasma glucagon levels of mice and that this effect is mediated by the peripheral serotonin2 (5-HT2) receptor. The present paper further investigated the involvement of serotonergic and catecholaminergic systems in hyperglucagonemia elicited by tryptamine. An inhibitor of 5-HT synthesis, p-chlorophenylalanine, did not affect tryptamine-induced increases in plasma glucagon levels. Tryptamine-induced hyperglucagonemia was not inhibited by adrenalectomy or by an inhibition of catecholamine synthesis by alpha-methyl-p-tyrosine. These findings indicate that tryptamine-induced hyperglucagonemia is elicited by its direct activation of 5-HT2 receptors and is not mediated by levels of endogenous 5-HT and catecholamines. The results further suggest that the peripheral 5-HT2 receptor has a possible role in the release of glucagon.

Adrenalectomy↗
PubMed1984

The distribution and turnover of tryptamine in the brain and spinal cord.

Tryptamine levels have been determined in mouse brain regions and spinal cord and in rat spinal cord. They were; caudate nucleus 2.5 ng X g-1, hypothalamus less than 0.5 ng X g-1, hippocampus less than 0.7 ng X g-1, olfactory bulb less than 0.7 ng X g-1, olfactory tubercles less than 0.6 ng X g-1, brain stem less than 0.4 ng X g-1, cerebellum less than 1.0 ng X g-1, and the "rest" 0.9 ng X g-1. The mouse whole brain was found to have 0.5 ng X g-1, the mouse spinal cord 0.3 ng X g-1, and the rat spinal cord 0.3 ng X g-1. These concentrations increased rapidly to 22.8 ng X g-1, 14.2 ng X g-1, and 6.6 ng X g-1 respectively at 1 hr after 200 mg X kg-1 pargyline. The turnover rates and half lives of tryptamine in the mouse brain and spinal cord and rat spinal cord were estimated to be 0.14 nmol X g-1 X h-1 and 0.9 min; 0.054 nmol X g-1 X h-1 and 1.5 min and 0.04 nmol X g-1 X h-1 and 1.6 min respectively. The aromatic L-aminoacid decarboxylase inhibitors NSD 1034 and NSD 1055 reduced synthesis of tryptamine in controls and pargyline pretreated animals. Tryptophan increased the concentrations of mouse striatal tryptamine and 5-hydroxytryptamine and brain stem 5-hydroxyindole acetic acid. p-Chlorophenylalanine reduced formation of 5-hydroxytryptamine and 5-hydroxyindoleacetic acid but did not change that of tryptamine.

Animals↗
PubMed1988

The hypoglycemic effects of tryptamine in mice: mediation by 5-HT receptors.

The effects of tryptamine on blood glucose levels were studied. Tryptamine induced significant hypoglycemia in mice. The hypoglycemia elicited by tryptamine was strongly antagonized by methysergide, an antagonist of both 5-HT1 and 5-HT2 receptors. A 5-HT2 receptor antagonist, ketanserin, partially inhibited the tryptamine-induced hypoglycemia. These results suggest that tryptamine-induced hypoglycemia is mediated by 5-HT1 and 5-HT2 receptors.

Animals↗
PubMed1992

Hyperglucagonemia induced in mice by tryptamine: involvement of the peripheral 5-HT2 receptors.

The effects of an indoleamine, tryptamine, on plasma glucagon levels were investigated in mice. Tryptamine induced dose-related increases in plasma glucagon levels. The hyperglucagonemia effects of tryptamine were completely antagonized by methysergide and ketanserin which have a high affinity to 5-HT2 receptors. In addition, the peripheral 5-HT2 receptor antagonist, xylamidine, also strongly inhibited tryptamine-induced hyperglucagonemia. Our results indicate that the peripheral 5-HT2 receptors mediate the increase in plasma glucagon levels induced by tryptamine and that these receptors may have a role in the control of glucagon secretion.

Animals↗