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PubMed2000

Tryptamine derivatives as non-competitive N-methyl-D-aspartate receptor blockers: studies using [(3)H]MK-801 binding in rat hippocampal membranes.

Derivatives of phenylethylamine and tryptamine share structural features with the non-competitive N-methyl-D-aspartate (NMDA) receptor blockers phencyclidine, ketamine, and MK-801. Tryptamine and phenylethylamine inhibited the specific binding of [(3)H]MK-801 to rat hippocampal membranes with IC(50)'s 190 and 905 microM, respectively. The corresponding amino acids phenylalanine and tryptophan were inactive, their methyl esters, however, were slightly more potent than the amines. The methyl ester of the naturally occurring L-tryptophan was 12 times more potent than the methyl ester of the D-isomer, whereas the corresponding isomers derived from phenylalanine exhibited no stereoselectivity. The potency of tryptamine was increased by substitutions as, e.g. in 5-methyltryptamine (IC(50) 12 microM) and tryptophan octylester (IC(50) 5.2 microM). Compounds formed in vivo from L-tryptophan and a lipophilic counterpart may function as endogenous non-competitive NMDA receptor blockers.

Amphetamine↗
PubMed1986

Sensitive determination of deuterated and non-deuterated tryptophan, tryptamine and serotonin by combined capillary gas chromatography and negative ion chemical ionization mass spectrometry.

Sensitive methods for the determination of deuterated and non-deuterated tryptophan, tryptamine and serotonin by combined capillary gas chromatography and negative ion chemical ionization mass spectrometry were developed. [3,3-2H2]-L-Tryptophan, which was used as a tracer, was synthesized for studies of their in vivo metabolism. Tryptophan was converted into its trifluoroacetylmethyl derivative after prepurification with an AG 50W-X2 cation-exchange column. Tryptamine and serotonin were extracted with 20% butanol in diethyl ether and derivatized with trifluoroacetic anhydride. These derivatives were separated and determined by selected ion monitoring. In these determinations, [2',3,3,4',5',6',7'-2H7]-D,L-tryptophan, [alpha,alpha,beta,beta-2H4]tryptamine and [alpha,alpha,beta,beta-2H4]serotonin were used as internal standards.

Chemical Phenomena↗
PubMed1997

Application of tryptamine as a derivatizing agent for the determination of airborne isocyanates. Part 7. Selection of impinger solvents and the evaluation against dimethyl sulfoxide used in US NIOSH Regulatory Method 5522.

The application of tryptamine to derivatize airborne isocyanates has been evaluated and adopted by the National Institute for Occupational Safety and Health (NIOSH) as the latest isocyanates regulatory method (Method 5522) in the USA. Method 5522 uses dimethyl sulfoxide (DMSO) as the impinger solvent in which tryptamine is dissolved to sample isocyanates for analysis. Since DMSO is both extremely hygroscopic and corrosive, it is not a satisfactory solvent for impinger air sampling of isocyanates. The high boiling and freezing points also present some distinct drawbacks. In a search for a suitable impinger solvent, the efficiencies of various solvents, which all were potentially more suitable for sampling isocyanates viz., N,N'-dimethylformamide, butyl acetate, isobutyl acetate, sec-butyl acetate, tert-butyl acetate and octane, were investigated. Simulated air sampling was conducted on two commonly used isocyanates in industry, hexamethylene diisocyanate (HDI) and toluene diisocyanate (TDI), which were vaporized and sampled into impingers containing dissolved tryptamine. Butyl acetate and octane were found to be most suitable for using as impinger solvents. Recoveries of isocyanates at two concentration levels of HDI and TDI were 93.4-108% in comparison with those of using DMSO.

Air Pollutants, Occupational↗
PubMed1966

On the ability of Taphrina deformans to produce indoleacetic acid from tryptophan by way of tryptamine.

The metabolism of tryptophan by Taphrina deformans has been studied to confirm the reported ability of this organism to produce tryptamine. Such amine production was not observed, despite use of amine oxidase inhibitors at levels which should have resulted in the accumulation of tryptamine in the medium. It has been shown that the metabolites of tryptophan include indolepyruvic acid, indolelactic acid, tryptophol, and indoleacetic acid, and that the original report of tryptamine production must be reevaluated in light of the extraction procedures employed.

Ascomycota↗
PubMed1986

The classification of peripheral 5-HT2-like receptors using tryptamine agonist and antagonist analogues.

In a previous study, we attempted to verify the classification of 5-hydroxytryptamine2 (5-HT2) receptors in three vascular tissues, by use of the conventional antagonists, ketanserin, spiperone, methysergide and trazodone. However, it was not possible to conclude homogeneity of the receptor type in the three tissues due to the inconsistent behaviour of these antagonists, in particular, their apparently variable affinities between the tissues. These results led to the reliability of the conventional antagonists being questioned as receptor probes. In the present study, a set of tryptamine analogues were investigated in two of the tissues, the rabbit aorta and the rat jugular vein. Unlike the conventional antagonists, these compounds bear a close chemical relation to the natural agonist, 5-HT. In both tissues, alpha, alpha-dimethyltryptamine demonstrated apparently simple competitive antagonism of 5-HT-induced constrictions. Its affinity was estimated to be the same in each case. The affinities and relative efficacies of 5-HT, 5-cyanotryptamine, N,N-dimethyltryptamine and N-benzyl-5-methoxytryptamine were also found to be indistinguishable between the two tissues. Unlike the conventional 5-HT2 receptor antagonists, these tryptamine analogues failed to distinguish between the 5-HT receptors in the rabbit aorta and rat jugular vein implying that they truly belong to the same class. In view of this result, it is suggested that simple tryptamine analogues are more reliable probes for 5-HT receptor classification than ligands which bear little or no chemical relation to the natural agonist.

Animals↗
PubMed1994

Comparison of the effects of IVth ventricular administration of some tryptamine analogues with those of 8-OH-DPAT on autonomic outflow in the anaesthetized cat.

1 The present study compares the effects on representative autonomic outflows of IVth ventricular application of tryptamine analogues which act at 5-HT1 receptors with 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT). 2 Cumulative doses of 8-OH-DPAT, N,N-di-n-propyl-5-carboxamidotryptamine (DP-5-CT) and 5-carboxamidotryptamine (5-CT, 2.5-40 nmol kg-1), sumatriptan (10-160 nmol kg-1), indorenate (100-800 nmol kg-1), 5-hydroxytryptamine (5-HT, 20-640 nmol kg-1) both alone and in the presence of cinanserin (0.1 mg kg-1) were given into the IVth ventricle of cats which were anaesthetized with a mixture of alpha-chloralose and pentobarbitone sodium, neuromuscularly blocked and artificially ventilated. Recordings were made of arterial blood pressure, heart rate, renal, cardiac, splanchnic and phrenic nerve activities, femoral arterial flow, tracheal and intragastric pressures. 3 Central application of each of the agonists evoked significant falls in arterial blood pressure. In addition 8-OH-DPAT, DP-5-CT, 5-CT and 5-HT all evoked a differential inhibition of sympathetic nerve activities, with renal nerve activity being the most sensitive and cardiac nerve activity the least sensitive. In the dose-ranges used, administration of sumatriptan evoked reductions only in renal and splanchnic nerve activities whilst indorenate reduced activity in all three sympathetic nerves to a similar extent. 4. The effect of the agonists on heart rate was more inconsistent than the effects on sympathetic outflow.IVth ventricular application of 5-CT and sumatriptan were without effect on heart rate whilst 8-OH-DPAT, DP-5-CT, indorenate and 5-HT alone and in the presence of cinanserin all evoked significant bradycardias. However, whilst atropine partially reversed the bradycardias evoked by 8-OHDPAT and only slightly reversed those caused by indorenate, atropine was without effect on those evoked by DP-5-CT or 5-HT.5. None of the analogues tested had significant effects on gut motility, phrenic nerve discharge or tracheal pressure. 8-OH-DPAT, DP-5-CT, indorenate and 5-HT were without effect on femoral arterial conductance. However, following pretreatment with cinanserin, 5-HT evoked a significant reduction in femoral arterial conductance. At its highest dose, sumatriptan evoked a significant increase in femoral arterial conductance as did 5-CT at the 20 nmol kg-1 dose.6. It is concluded that the present data support the view that 5-HT1A receptors at the level of the brainstem are involved in the central sympathoinhibitory effects caused by intravenous administration of 5-HT1A agonists. Further, brainstem 5-HT1A receptors play an important role in the control of renal sympathetic outflow while brainstem 5-HT2 receptors are involved in the control of skeletal muscle and/or skin blood flow. Selective tryptamine agonists for 5-HT1A receptors differ from non-tryptamine agonists in that they do not cause an increase in central cardiac vagal tone.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1979

Gastric emptying and secretion in the calf on duodenal infusion of tryptophan, tryptamine and 5-hydroxytryptamine.

1. Gastric emptying, gastric acid and pepsinogen secretion were assessed simultaneously in the conscious calf using the test meal and duodenal perfusion technique (Bell & Mostaghni, 1975).2. When 60 mM-HCl was infused into the duodenum, gastric emptying was arrested but both acid and pepsinogen secretion continued at a low level. Duodenal infusion with isotonic NaHCO(3) caused rapid exponential emptying of the test meal and acid and pepsinogen output was more than doubled.3. Duodenal infusion of amino acids in isotonic NaHCO(3) did not affect the rapid emptying, except infusion with tryptophan, which caused a measureable degree of inhibition of emptying, with concomitant effects on acid and pepsinogen secretion4. Tryptamine and 5-hydroxytryptamine (5-HT) incorporated in low concentration into isotonic NaHCO(3) also produced depression of gastric emptying, acid and pepsinogen levels comparable to the response initiated by acid infusate. Tryptophan was effective only in non-physiological amounts while 5-HT and tryptamine were active in smaller doses.5. Our results suggest that the inhibition of gastric emptying following duodenal infusion of tryptophan noted by Stephens, Woolson & Cooke (1975) may be due to the duodenal synthesis of its biogenic amine derivatives tryptamine and 5-HT.6. The level of activity of the three gastric functions, emptying, acid secretion and pepsinogen secretion appears to be linked. A single stimulus, therefore, could evoke a duodenal receptor or receptors to mediate or suppress activity of the gastric smooth muscle and secretory cells through interrelated mechanisms. The effect of some duodenal infusates, however, produces some variability in response which suggests differential activation of different receptors with consequent variable motor activity on effector cells.

Amino Acids↗
PubMed1989

The evidence for the involvement of the 5-HT1A receptor in 5-HT syndrome induced in mice by tryptamine.

The involvement of the 5-HT1A receptor in the 5-HT syndrome (head weaving and hindlimb abduction) induced in DBA mice by tryptamine was investigated. Methysergide, (-)propranolol and spiperone suppressed both the head weaving and hindlimb abduction induced by tryptamine. However, ketanserin and ICS 205-930 did not affect them. Haloperidol induced small decreases in the head weaving, but had no effect on the hindlimb abduction. These results indicate that the 5-HT syndrome induced by tryptamine in mice is mediated by the 5-HT1A receptor. Therefore, 5-HT syndrome may also be associated with the 5-HT1A receptor in mice, as it is in rats.

Animals↗
PubMedDate not supplied

13C NMR investigations on the stacking of 5'-AMP with tryptamine.

Complex formation between 5'-adenosine monophosphate (5'-AMP) and tryptamine was investigated by measuring 13C chemical shifts and spin-lattice relaxation times. The chemical shift changes observed were attributed to ring current effects originating in the stacking of the two respective aromatic moieties and to puckering changes of the AMP ribose. Differences in the magnitude of the shifts of the aromatic carbons were related to the geometry of the complex and compared with those found for AMP selfassociation. Upon complex formation the relaxation times of especially the tryptamine indole carbons were greatly reduced, this was explained by an increase in the particle size. Small changes found for the AMP carbons in solutions without tryptamine result from AMP selfassociation. Deviations from isotropic motion observed for the non-aromatic moieties are discussed.

Adenosine Monophosphate↗
PubMed1989

Serotonin and tryptamine metabolism in the acute hepatic failure model: changes in tryptophan and its metabolites in the liver, brain and kidney.

When heat-killed Propionibacterium acnes, a gram-positive anaerobe, is intravenously injected into mice followed by an intravenous injection of gram-negative lipopolysaccharide (LPS) 7 days later, most of the mice die of massive hepatic cell necrosis within 24 hours of LPS injection. Using this experimental model, acute hepatic failure was induced in mice, and the tryptophan metabolism in the liver, brain and kidney was studied. As a result, the tryptophan level was remarkably high in all three organs, and the metabolism of both the tryptamine pathway and serotonin pathway was induced. However, in the brain, the tryptamine metabolism was more induced compared to the serotonin, suggesting that the metabolites of tryptamine, may be involved in hepatic encephalopathy.

Acute Disease↗
PubMed1989

Tryptamine alkaloid toxicosis in feedlot sheep.

Tryptamine alkaloid toxicosis (Phalaris staggers) was diagnosed in feedlot sheep. Clinical signs of toxicosis, which were exacerbated by excitement, included gait abnormalities, muscular tremors, nystagmus, and convulsions. An estimated 8% of the most severely affected lambs had clinical signs of toxicosis. Gross lesions detected in the brain of affected lambs consisted of focal gray-green discoloration in the brain stem and thalamus; these areas had microscopic evidence of intraneuronal pigment accumulation. Brain specimens obtained at slaughter indicated that 60% of the lambs had lesions consistent with tryptamine alkaloid toxicosis. Tryptamine alkaloids were found in low concentrations in the feed. Lambs exposed to these feeds had higher death losses than those that were not exposed to the feeds. Cobalt concentration in the feed was higher than that previously reported to be associated with Phalaris staggers.

Alkaloids↗
PubMedDate not supplied

Synthesis of N-nicotinoyl-tryptamine (tryptamide).

N-Nicotinoyl-tryptamine was synthetized by acylation of tryptamine with mixed nicotinic anhydride. The synthesis of tryptamine via DL-tryptophan decarboxylation in cyclohexanol, in the presence of tetraline oxidation products as the catalyst, was described as well.

Acylation↗
PubMed1985

5-Hydroxytryptamine receptor in isolated rabbit aorta: characterization with tryptamine analogs.

The 5-HT2 receptor in isolated rabbit thoracic aorta was characterized by examining the relationships between structure and activity of nine tryptamine analogs. All assays were conducted after blockade of the alpha adrenergic receptor and inactivation of the neuronal uptake-1 system and monoamine oxidase. Seven of the analogs tested were agonists. 6-Hydroxytryptamine and 7-hydroxytryptamine showed little or no agonist activity in this preparation. The pA2 of spiperone was independent of the agonist assayed and defined the receptor activated by each agonist as the 5-HT2 receptor. The dissociation constant (KA) and relative intrinsic efficacy were determined for each agonist. The KA and relative intrinsic efficacy values for 5-hydroxytryptamine were 0.25 microM and 1, respectively. The KA and relative intrinsic efficacy values for 5-methoxytryptamine were 0.14 microM and 0.86, respectively, and were not significantly different from those for 5-hydroxytryptamine. The other five analogs were partial agonists. N-Methyl-5-hydroxytryptamine and bufotenine had relative intrinsic efficacies of about 0.3 and KA values not statistically different from the KA value for 5-hydroxytryptamine. Tryptamine, 5-methyltryptamine and alpha-methyl-tryptamine had KA values of about 1 microM and relative intrinsic efficacies of 0.6, 0.6 and 0.4, respectively. These results revealed the differential effects of structural changes on drug affinity and intrinsic efficacy. This information will be applicable in the design of selective agonists or antagonists for the classification of less well defined 5-hydroxytryptamine receptors.

Animals↗
PubMed1984

Central tryptamine turnover in depression, schizophrenia, and anorexia: measurement of indoleacetic acid in cerebrospinal fluid.

There has been a continuing interest in the possible role of the trace amine tryptamine in the etiology of neuropsychiatric disorders. We have therefore examined cerebrospinal fluid (CSF) levels of indole-3-acetic acid (IAA), the major metabolite of tryptamine, in a large group of normals and in several patient populations. No differences in CSF IAA levels (ng/ml, mean +/- SEM) were observed between normals (4.39 +/- 0.37, n = 36), anorectics (4.40 +/- 0.42, n = 35), schizophrenics (4.06 +/- 0.05, n = 17), manics (4.32 +/- 0.63, n = 10), or depressives (5.23 +/- 0.49, n = 39). A significant elevation (p = 0.05) was found in the subgroup of retarded depressives (RDC) where levels of 5.90 +/- 0.80 (n = 19) were observed. An age effect (r = 0.39, p = 0.02, n = 36) was observed in normals; however IAA was not reduced to either height or weight. IAA tended to be higher (but not significantly) in females in all groups studied; this difference also was not significant when all diagnostic groups (except anorectics) were combined (female: 4.95 +/- 0.44, n = 45; male: 4.46 +/- 0.30, n = 66). In general, the results indicate that tryptamine turnover is not altered in the disorders studied. The functional significance of the slight elevation seen in retarded depressives is not clear.

Adult↗
PubMed1978

Comparison of the X537A-induced ionophoric removal of serotonin and tryptamine from intact human platelets.

In the absence of appreciable dense-body release from platelets, X537A causes rapid movement of 90--95% of vesicular H3-5HT into the extracellular medium. X537A can in addition transport to the extracellular medium 20% of the total tryptamine sequestered in platelets. Investigation of the extraction of aqueous 5HT and tryptamine into a chloroform phase, and the subsequent extraction of each of the two amines from a chloroform to an aqueous phase, suggest that 5HT, but not tryptamine, is transported efficiently between aqueous phases through a non-polar solvent. The observed differences in the movement of the two amines through platelet membranes may be attributable to a similar phenomenon.

Anti-Bacterial Agents↗
PubMed1980

Urinary tryptamine excretion in chronic schizophrenics with low platelet MAO activity.

Reduced platelet MAO activity has been previously reported as a biochemical marker for a subgroup of psychiatric patients, including some chronic schizophrenics. As tryptamine metabolism appears to be sensitive to alterations in MAO activity, urinary tryptamine excretion was measured in chronic schizophrenics with low platelet MAO activity, chronic schizophrenics with normal platelet MAO activity, and age-matched and sex-matched controls. The increased urinary tryptamine excretion observed in chronic schizophrenics with low platelet MAO activity may reflect a pathophysiologic mechanism associated with low MAO activity.

Adult↗
PubMed1997

Tryptamine: a possible endogenous substrate for CYP2D6.

The fact that CYP2D6 is not only expressed in liver but also in brain and the clinical association of this cytochrome with Parkinson's disease suggests the possibility of existence of some endogenous substrate, and among these perhaps one or more neurotransmitters could be metabolized by CYP2D6. In this study we explored such a possibility by studying the modulation of CYP2D6 activity by several neurotransmitters. Our findings confirm the occurrence of a competitive inhibition of dextromethorphan O-demethylation in the presence of tryptamine, with a Ki value of 44.6 microM. Tryptamine was metabolized in human liver microsomes by an enzyme activity with a K(m) of 3.6 +/- 0.9 microM. Such activity is NADPH dependent and is inhibited by quinidine and CYP2D6-specific substrates. The product of the reaction is tryptophol. These results suggest that tryptamine may be an endogenous substrate of CYP2D6.

Cytochrome P-450 CYP2D6↗
PubMed1995

Tryptophan Decarboxylase, Tryptamine, and Reproduction of the Whitefly.

Tryptophan decarboxylase (TDC) from Catharanthus roseus (periwinkle) converts tryptophan to the indole-alkaloid tryptamine. When the TDC gene was expressed in transgenic tobacco, the 55-kD TDC enzyme and tryptamine accumulated. Bemisia tabaci (sweetpotato whitefly) reproduction on transgenic plants decreased up to 97% relative to controls. Production of tryptamine, its derivatives, or other products resulting from TDC activity may discourage whitefly reproduction and provide a single-gene-based plant protection strategy.

Journal Article↗