Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Tryptamines”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources
PubMed1984

Unique [3H]tryptamine binding sites in rat brain: distribution and pharmacology.

[3H]Tryptamine binding in rat brain is widely distributed with highest densities in the cortex, striatum and hippocampus. This binding is stereospecific and is potently displaced by tryptamine analogues and beta-carbolines. Phenethylamines also possess a weaker activity in displacing [3H]tryptamine. The strict structural requirements for binding to this site substantiate its unique character and suggest that it may represent a tryptamine receptor in the CNS.

Animals↗
PubMed2006

Tryptamine induces cell death with ultrastructural features of autophagy in neurons and glia: Possible relevance for neurodegenerative disorders.

Tryptamine derivatives are a family of biogenic amines that have been suggested to be modulators of brain function at physiological concentrations. However, pharmacological concentrations of these amines display amphetamine-like properties, and they seem to play a role in brain disorders. Amphetamines induce autophagy in nerve cells, and this type of cell death has also been involved in neurodegenerative diseases. In the present work, we clearly demonstrate for the very first time that high concentrations of tryptamine (0.1-1 mM) induce autophagy in HT22 and SK-N-SH nerve cell lines and in primary cultures of astrocytes, glial cells being less sensitive than neurons. Ultrastructural cell morphology shows all of the typical hallmarks of autophagy. There is no nuclear chromatin condensation, endoplasmic reticulum and mitochondria are swollen, and a great number of double-membraned autophagosomes and residual bodies can be shown in the cytoplasm. Autophagosomes and residual bodies contain mitochondria, membranes, and vesicles and remain unabridged until the cell membrane is disrupted and the cell dies. The same results have been found when cells were incubated with high concentrations of 5-methoxytryptamine (0.1-1 mM). Our results establish a possible link between the role of tryptamine derivatives in brain disorders and the presence of autophagic cell death in these kinds of disorders.

Animals↗
PubMed1989

Biotransformation of tryptamine derivatives in mycelial cultures of Psilocybe.

Mycelial cultures of Psilocybe cubensis capable of forming psilocybin and psilocin de novo display a high capacity for hydroxylation of tryptamine derivatives at the 4-position. A specific biotransformation of added synthetic N,N-diethyl-tryptamine was found. Thus high amounts of 4-hydroxy-N,N-diethyltryptamine (up to 3.3%) and a minor quantity of 4-phosphoryloxy-N,N-diethyltryptamine (0.01-0.8%) were isolated from fruiting bodies of Psilocybe cubensis in corresponding experiments. This is the first example of a directed biosynthesis of tryptamine substances by fungi. An effective biotransformation of N-methyltryptamine was also demonstrated with surface cultures of Psilocybe semilanceata. Baeocystin, a possible natural precursor of psilocybin, was detected and quantified in the biomasses. No alkaloids could be found in the culture medium.

Agaricales↗
PubMed1981

Tryptophan availability and the control of 5-hydroxytryptamine and tryptamine synthesis in human CNS.

The data presented here suggest that control of human brain 5HT synthesis by precursor availability is similar to that in the rat. Plasma tryptophan controls the brain level, although the plasma-brain relationship is modified by other large neutral amino acids in plasma. In normal circumstances brain tryptophan is an important factor controlling the synthesis of 5HT and tryptamine in human brain. However, the elevated brain tryptophan in patients with chronic liver disease does not lead to an increase in the rate of 5HT metabolism. In human brain the rate of tryptamine synthesis is normally aobut 10-20% of the rate of 5HT synthesis. Tryptamine metabolism is more sensitive than 5HT metabolism to changes in brain tryptophan. This is especially apparent after a tryptophan load. Our results suggest that tryptophan administration increases indoleamine function, as well as indoleamine synthesis, in depressed patients. Whether physiological variations in brain tryptophan in normal people are responsible for variations in indoleamine function is an open question.

Animals↗
PubMed1991

Effects of imipramine and some tryptamine derivatives on the efflux of 3H-5-hydroxytryptamine from rabbit platelets.

The efflux of 3H-5-hydroxytryptamine (3H-5-HT) from rabbit platelets (monoamine oxidase inhibited; pretreatment with reserpine) was measured in the absence and presence of various concentrations of imipramine or a number of tryptamine derivatives. The maximum efflux-accelerating effect (Emax) of 5-HT and some other tryptamines (e.g., N-methyl-5-HT, 5-methoxytryptamine) far exceeded that of imipramine, whereas the Emax for 2-methyl-5-HT did not. It is concluded that tryptamines that are more effective in releasing 3H-5-HT than imipramine have the property of being substrates of the 5-HT transporter.

Analysis of Variance↗
PubMed1984

Saturable uptake of [3H]-tryptamine in rabbit platelets is inhibited by 5-hydroxytryptamine uptake blockers.

[3H]-tryptamine is taken up by rabbit platelets through an active and saturable process which is temperature sensitive, sodium-dependent and inhibited by imipramine and non-tricyclic 5-hydroxytryptamine (5-HT) uptake blockers. There is an excellent correlation between the Ki for the inhibition of [3H]-tryptamine and [3H]-5-HT uptake in rabbit platelets for a series of 5-HT uptake blockers. These results indicate that [3H]-tryptamine is actively transported through the membrane of blood platelets by the same carrier that transports 5-HT.

Animals↗
PubMed1995

Overexpression of a tryptophan decarboxylase cDNA in Catharanthus roseus crown gall calluses results in increased tryptamine levels but not in increased terpenoid indole alkaloid production.

The enzyme tryptophan decarboxylase (TDC) (EC 4.1.1.28) catalyses a key step in the biosynthesis of terpenoid indole alkaloids in C. roseus by converting tryptophan into tryptamine. Hardly any tdc mRNA could be detected in hormone-independent callus and cell suspension cultures transformed by the oncogenic T-DNA of Agrobacterium tumefaciens. Supply of tryptamine may therefore represent a limiting factor in the biosynthesis of alkaloids by such cultures. To investigate this possibility, chimaeric gene constructs, in which a tdc cDNA is linked in the sense or antisense orientation to the cauliflower mosaic virus 35S promoter and terminator, were introduced in C. roseus cells by infecting seedlings with an oncogenic A. tumefaciens strain. In the resulting crown gall tumour calluses harbouring the tdc sense construct, an increased TDC protein level, TDC activity and tryptamine content but no significant increase in terpenoid indole alkaloid production were observed compared to empty-vector-transformed tumour calluses. In tumour calluses containing the tdc antisense construct, decreased levels of TDC activity were measured. Factors which might be responsible for the lack in increased terpenoid indole alkaloid production in the tdc cDNA overexpressing crown gall calluses are discussed.

Alkaloids↗
PubMed2001

Biotransformation of tryptamine and secologanin into plant terpenoid indole alkaloids by transgenic yeast.

A transgenic Saccharomyces cerevisiae was constructed containing the cDNAs coding for strictosidine synthase (STR) and strictosidine beta-glucosidase (SGD) from the medicinal plant Catharanthus roseus. Both enzymes are involved in the biosynthesis of terpenoid indole alkaloids. The yeast culture was found to express high levels of both enzymes. STR activity was found both inside the cells (13.2 nkatal/g fresh weight) and in the medium (up to 25 nkatal/l medium), whereas SGD activity was present only inside the yeast cells (2.5 mkatal/g fresh weight). Upon feeding of tryptamine and secologanin, this transgenic yeast culture produced high levels of strictosidine in the medium; levels up to 2 g/l were measured. Inside the yeast cells strictosidine was also detected, although in much lower amounts (0.2 mg/g cells). This was due to the low permeability of the cells towards the substrates, secologanin and tryptamine. However, the strictosidine present in the medium was completely hydrolyzed to cathenamine, after permeabilizing the yeast cells. Furthermore, transgenic S. cerevisiae was able to grow on an extract of Symphoricarpus albus berries serving as a source for secologanin and carbohydrates. Under these conditions, the addition of tryptamine was sufficient for the transgenic yeast culture to produce indole alkaloids. Our results show that transgenic yeast cultures are an interesting alternative for the production of plant alkaloids.

Biotechnology↗
PubMed1983

Antagonism by tetrahydro-beta-carboline of the vasoconstrictor responses to tryptamine in rat tail arteries.

Tryptamine and 5-HT mediate vasoconstriction in the isolated perfused rat tail artery. These agonists were differentiated by the classical serotonin receptor antagonists methysergide and ketanserin which were significantly more potent against 5-HT-induced responses. Neither prazosin nor RX 781094 alone or in combination reduced the vasoconstriction produced by tryptamine. Tetrahydro-beta-carboline (THBC) was devoid of agonist properties and behaved as a competitive antagonist of tryptamine but not of 5-HT. THBC also had alpha-adrenoceptor blocking properties in this preparation.

Adrenergic alpha-Agonists↗
PubMed1996

Formation of tetrahydroharman (1-methyl-1,2,3,4-tetrahydro-beta-carboline) by Helicobacter pylori in the presence of ethanol and tryptamine.

Helicobacter pylori contains alcohol dehydrogenase which oxidizes ethanol to acetaldehyde. In the present study, H. pylori cytosol was incubated in a buffered media at pH 6.0 and 7.4 in the presence of ethanol and tryptamine. Under these conditions, tetrahydroharman (1-methyl-tetrahydro-beta-carboline) was produced as a condensation product of tryptamine and acetaldehyde. At pH 6.0, 20.60 +/- 5.00% of the added tryptamine was converted to tetrahydroharman, while 27.00 +/- 4.80% (mean +/-SD) was converted at pH 7.4. Similar reactions between acetaldehyde and other dietary amines seem likely. Such biogenic alkaloids, if formed in vivo, might contribute to the dysphoric effects of alcohol.

Acetaldehyde↗
PubMed1985

Effects of quipazine and of tryptamine on self-stimulation of median raphé nucleus and of lateral hypothalamus in rats.

Separate groups of male Wistar rats were trained to lever press on a continuous reinforcement schedule under which behaviour was maintained by electrical stimulation of the median raphé nucleus (N = 6) or the lateral hypothalamus (N = 6). The effects of several doses of quipazine (2.5-7.1 mg/kg) and of tryptamine (10-80 mg/kg) were assessed with each group. Administration of quipazine resulted in a decrease of median raphé self-stimulation at 5.0 and 7.1 mg/kg. This compound had no statistically significant effect on lateral hypothalamic self-stimulation. Administration of tryptamine resulted in significant decreases in self-stimulation at both sites, however, whereas the effects of this drug were significant at 20, 40 and 80 mg/kg with median raphé self-stimulation, a significant decrease in lateral hypothalamic self-stimulation was only observed at 80 mg/kg. As baseline response rates differed in the two self-stimulation sites, a second group of animals with lateral hypothalamic sites (n = 6) were tested with quipazine (2.5-7.1 mg/kg) at an overall baseline response rate matched to that of the median raphé group. Although a tendency to decrease self-stimulation rates was found in this group, these results were not significant. These data suggest, therefore, that median raphé self-stimulation is more sensitive than lateral hypothalamic self stimulation to disruption by the effects of quipazine and tryptamine.

Animals↗
PubMed1985

Membrane responses and changes in cAMP levels in Aplysia sensory neurons produced by serotonin, tryptamine, FMRFamide and small cardioactive peptideB (SCPB).

While recent evidence indicates a role for serotonin (5-HT) in modulating the defensive tail-withdrawal reflex in Aplysia, little information exists concerning the specificity of these 5-HT effects. As a first-step in addressing this issue we have examined the dose-response relationship for one aspect of the 5-HT modulation (enhancement of cAMP levels in isolated clusters of sensory neurons) and compared the effects of 5-HT with three potential neurotransmitters: tryptamine, FMRFamide (Phe-Met-Arg-Phe-NH2) and small cardioactive peptideB (SCPB). Cyclic adenosine monophosphate (cAMP) levels were enhanced as a graded function of the concentration of 5-HT with an EC50 of 14 microM. At a concentration of 5 microM, both 5-HT and SCPB produced nearly identical increases in the cAMP content of sensory neurons. In contrast, 5 microM tryptamine or 5 microM FMRFamide had little or no effect on cAMP levels. We also examined the effects of these agents on membrane currents and membrane conductance. Both 5-HT and SCPB produced an inward current associated with a decrease in input conductance. Tryptamine had little or no effect, while FMRFamide produced a response opposite to that of 5-HT and SCPB; an outward current associated with an increase in membrane conductance.

Animals↗
PubMed1980

Tryptamine-adenosine 5'-monophosphate interactions as studied by nuclear magnetic resonance and relaxation.

The conformation of tryptamine-adenosine 5'-monosphate and of their 1:1 complex in neutral aqueous solution at 297 K has been investigated by proton NMR and relaxation. The dependences of the proton chemical shift as a function of the tryptamine and AMP concentrations yield an association constant of 6.5 +/- 0.5 1 . mol-1. The reorientation correlation time of the complex tau R = (2.5 +/- 0.1) . 10(-10) s has been determined from the deuteron and ESR linewidth measurements on specifically labelled AMP. The proton longitudinal relaxation shows that the adenine and indole rings are head-to-head stacked 0.31 +/- 0.01 nm apart as confirmed by proton chemical shift measurements. In this complex, the AMP ribose ring takes the 3'-endo (N) conformation and the orientation of the adenine base is anti, whereas the tryptamine aminoethyl residue, in the gauche conformation, is most likely bound to the phosphate by coulombic interactions.

Adenosine Monophosphate↗
PubMed1982

Tryptamine modifies cortical neurone responses evoked by stimulation of nucleus raphe medianus.

Electrical stimulation of 5-hydroxytryptamine (5-HT) containing cell bodies in the nucleus raphe medianus (NRM) evoked complex responses on most cortical neurones. The predominant response pattern was biphasic, a short latency inhibition being followed by a long latency excitation. Occasional cells showed a third phase, a very long latency weak inhibition. When tryptamine was applied iontophoretically with ejecting currents which did not alter cell firing rate the excitatory effects of NRM stimulation were profoundly reduced. The initial inhibition of cell firing was not altered by tryptamine but some evidence suggested that the long latency inhibition could be potentiated. The results may suggest that tryptamine can modify the neuronal effects of synaptically released 5-hydroxytryptamine.

Animals↗
PubMed2004

An analytical perspective on favoured synthetic routes to the psychoactive tryptamines.

Many tryptamine derivatives are known to induce altered states of consciousness and are increasingly of interest in forensic and neurobiological studies. The analytical chemistry of certain synthetic routes to the tryptamines is discussed and likely side products and impurities identified, where literature reports are available. Recent examples from the authors' laboratory are presented to highlight future prospects and implications for analytical procedures. The aim of this review is to provide the analytical chemist with the foundation chemistry and some analytical targets to be able to undertake direct characterisation of products and intermediates. These might become available from interdiction of clandestine operations in a forensic environment or during the synthesis of the tryptamines for investigative neurobiological and clinical procedures.

Chemistry Techniques, Analytical↗
PubMed1987

Degradation of tryptamine in pig brain: identification of a new condensation product.

Incubation of tryptamine with pig brain homogenate led to the formation of a product which is not identical with other known tryptamine metabolites. The same results were observed with rat brain tissue and bovine brain tissue. The compound has been isolated and identified by NMR spectroscopy, fast atom bombardment mass spectroscopy, and by chemical synthesis as a thiazolidine derivative, (4R)-2-(3-indolylmethyl)-1,3-thiazolidine-4-carboxylic acid. It is formed by a condensation reaction of indole-3-acetaldehyde generated enzymatically from tryptamine and of free L-cysteine present in the tissue. The compound inhibited monoamine oxidase (preferentially type A) and the neuronal gamma-aminobutyric acid uptake.

Aldehydes↗
PubMed1984

Capillary column gas-liquid chromatography selected ion monitoring assay for [13C, 15N]N-methyltryptamine in human urine: failure to detect conversion of [13C,15N]tryptamine in schizophrenia patients.

A capillary column gas-liquid chromatography selected ion monitoring-based method was developed for the measurement of [13C,15N]N-methyltryptamine ( NMT ) in human urine. The method was employed to establish the extent of conversion of [13C,15N]tryptamine to the correspondingly labeled NMT in schizophrenic patients in an attempt to demonstrate whether methylation of tryptamine plays a role in schizophrenia. Mass spectrometric detection in the assay procedure is via chemical ionization (Isobutane) with monitoring of the MH+ ions of the trimethylsilyl derivatives of [13C,15N] NMT and the internal standard, [2H3,13C,15N] NMT . The assay possesses a sensitivity limit (using 200 ml of urine) of ca. 0.1 ng/ml, corresponding to substrate conversion of ca. 0.00005% with a 75 mg dose (i.v.) of labeled tryptamine. Evidence for methylation was found with only one of seven patients studied; the extent of substrate conversion for the one individual was only 0.0001%. These results do not support the indoleamine--methylation hypothesis of schizophrenia.

Adult↗
PubMed1997

Mutations of transmembrane IV and V serines indicate that all tryptamines do not bind to the rat 5-HT2A receptor in the same manner.

Two mutations of the rat serotonin 5-HT2A receptor were made, expressed and examined for their ability to bind and be stimulated by certain tryptamines as well as their ability to bind antagonists. Mutation of Ser207 to an Ala (S207A) resulted in no substantial changes in binding of either 5-HT2A antagonists or agonists. In contrast, mutation of Ser239 to an Ala (S239A) resulted in significant changes in the 5-HT2A receptor with some but not all agonists and antagonists examined. Specifically, 5-HT had decreased affinity for the S239A mutated 5-HT2A receptor, showing over a 10-fold decrease in receptor-binding displacement, while still being capable of stimulating IP3 formation. However, the agonists tryptamine, 5-methoxytryptamine (5-MeOT), and N-1-isopropyl-5-methoxytryptamine; and the antagonists ketanserin, LY 86057, and LY 53857 were significantly less affected by a S239A mutation. These results suggest that while 5-HT might have a direct interaction with the Ser239 of the 5-HT2A receptor, tryptamine and 5-MeOT interact with this receptor in a different manner.

Amino Acid Sequence↗