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PubMed1979

Factors altering platelet monoamine oxidase. The influence of oral glucose intake.

The specific activity of human platelet monoamine oxidase from control subjects undergoing glucose tolerance tests is reduced drastically. Three hours after intake of 100 g of glucose only 25%-30% of the MAO-baseline activity was measured with tryptamine. beta-phenylethylamine and p-tyramine as substrates. At about 5 hr, platelet MAO activity has increased again. Inhibition was not due to small molecular weight inhibitors or other diffusible factors. Studies of other platelet enzymes, including succinate dehydrogenase and isocitrate dehydrogenase (NADP+ dependent) showed no parallel reductions; hGH, insulin, blood glucose and platelet glycogen concentrations did not correlate with platelet MAO activity. The changes of MAO activity in respect with p-tyramine and tryptamine as substrates 24 hr after glucose ingestion suggest changes of the lipid microenvironment of this enzyme of the outer mitochondrial membrane.

Adult↗
PubMed1987

Selective beta-antagonists are equally and highly potent at 5-HT sites in the rat hippocampus.

Serotonin (5-hydroxytryptamine, 5-HT) and various tryptamine-related drugs were equi-potent to known beta-antagonists in competition experiments of 125Iodo-cyanopindolol binding in the rat hippocampus. IC50 values for all the tryptamine related drugs (5,7-DHT, 5-MT, 5-MEO, DMT) were very similar to those obtained for (-)-propranolol, (+/-)-cyanopindolol, zinterol and atenolol and were all in the nanomolar range. Saturation experiments demonstrated that in the rat hippocampus, a subpopulation of serotonin recognition sites comprised 50% of 125I-CYP binding. The KD was 140 +/- 30 pM and the Bmax was 71 +/- 7 fmole/mg protein. This suggests that 125I-CYP binding studies for the quantitation of beta-adrenergic receptors should be re-evaluated and caution should be exercised in the choice of the displacing agent for the definition of non-specific binding. (+/-)-[125Iodo]cyanopindolol (I-CYP) has been used as a radioligand which binds with high affinity and specificity to beta-adrenoceptors (Engel, Hoyer, Berthold and Wagner, 1981). The reported low dissociation constant (27-40 pM) of 125I-CYP for beta-adrenoceptors in various tissues, in combination with its high specific radioactivity (2175 Ci mmole-1) allowed binding studies to be carried out with low protein and ligand concentrations. These factors have established 125I-CYP as the choice ligand for the quantitation of beta-adrenoceptors in our laboratory (Edwards and Henn, 1985).(ABSTRACT TRUNCATED AT 250 WORDS)

5,7-Dihydroxytryptamine↗
PubMed1987

The serotonin (5-HT) autoreceptor in the hippocampus of the rabbit: role of 5-HT biophase concentration.

Slices of hippocampus from the rabbit were preincubated with [3H]5-HT), then superfused continuously and twice stimulated electrically. The stimulation-evoked overflow of tritium was inhibited by the 5-HT autoreceptor ligands 5-carboxamido-tryptamine (5-COHT), 5-HT, 5-methoxy-N,N-dimethyl-tryptamine (5-MeOMT), (+/-)-8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), methysergide and (+/-)-cyanopindolol in a concentration-dependent manner. These effects were competitively inhibited by the 5-HT autoreceptor antagonists, metitepin and metergoline. (+/-)-Cyanopindolol also reduced the evoked release of 5-HT from slices of cortex from the rat. The inhibitor of the uptake of 5-HT, 6-nitroquipazine diminished the autoreceptor-mediated depression of release of 5-HT. In cortex tissue from the rat, 6-nitroquipazine reversed the decreased release of 5-HT, due to (+/-)-cyanopindolol, to a facilitation. The disinhibition of the release of 5-HT by autoreceptor antagonists was further enhanced by 6-nitroquipazine. Non-linear regression analysis of concentration-response curves for 5-COHT yielded the following pKd of endogenous 5-HT at the autoreceptor: 7.753 +/- 0.116. This value corresponds to the pKd of 5-HT at the 5-HT1B binding site. The 5-HT biophase concentration at the autoreceptor of 10(-8.220 +/- 0.132)M was markedly enhanced by 6-nitroquipazine (10(-6)M) to 10(-7.476 +/- 0.132)M. It is concluded that the 5-HT autoreceptor belongs to the 5-HT1B subtype of receptor; the corresponding 5-HT biophase concentration can be estimated quantitatively; 8-OH-DPAT decreased the evoked release of 5-HT through both 5-HT autoreceptors and alpha 2-heteroreceptors and (+/-)-cyanopindolol acts as partial agonist at the 5-HT autoreceptor.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1976

The tryptolines: effect of intraventricular administration on spontaneous motor activity of rats.

The pharmacologic properties of the tryptolines, hindered analogues of the tryptamines, were studied behaviorally in rats. Following intraventricular injections, it was found that spontaneous motor activity decreased markedly during the initial 25 mins when compared with saline. Since both the tryptolines and tryptamines have been shown to be inhibitors of 5-hydroxytryptamine uptake, it may be possible that these compounds are acting indirectly throught an effect on the serotonergic system.

Animals↗
PubMed1978

Role of the periaqueductal gray substance in the antianxiety action of benzodiazepines.

In order to study the interactions between serotonergic mechanism and electrical stimulation of the mesencephalic central gray substance, rats were trained to lever-press for terminating aversive electric stimuli applied at the Periaqueductal gray and adjoining tectum of the mesencephalon. Experimental sessions consisted of 40 discrete escape trials of a maximum of 30 sec duration, separated by 30 sec intervals. Dose-effect curves of two tryptamine antagonists, cyproheptadine and methysergide, as well as of the benzodiazepine minor tranquilizer, chlordiazepoxide, on average escape latencies and on frequency distribution of individual latencies were determined. Doses of 3 to 10 mg/kg of cyproheptadine decreased average latencies of escape responding in six of eight rats studied. Doses of 10 and 30 mg/kg of methysergide also facilitated escape responding in one of three rats. In contrast, doses from 1 to 10 mg/kg of chlordiazepoxide, that cause little sedation or ataxia, produced dose-dependent increases in escape latencies. Furthermore, doses of 5.6 and 10 mg/kg of chlordiazepoxide partially blocked escape responding. The facilitatory effects of the tryptamine antagonists suggest that escape behavior is inhibited by brain tryptaminergic mechanisms, whereas the specific depressant effect of chlordiazepoxide on escape from Periaqueductal gray electrical stimulation suggest that this region may be involved in the antianxiety action of benzodiazepines.

Animals↗
PubMed1983

The discrepancy between the cross-reactivity of a monoclonal antibody to serotonin and its immunohistochemical specificity.

The rat monoclonal antibody YC5/45 has been shown to react specifically with serotonin containing neurones, and does not detect dopamine containing sites. On the other hand the monoclonal antibody recognizes dopamine, since it is capable of inhibiting the binding of 3H-YC5/45 to sheep red blood cells coated with serotonin albumin conjugate, or the direct agglutination of the same cells by the monoclonal antibody. Tryptamine and 5-methoxytryptamine are even better inhibitors, while derivatives with a modified-CH2-CH2-NH2 group are inactive. Treatment of the active compounds with paraformaldehyde increases their efficiency dramatically. The binding of antibody was also tested by cross linking with paraformaldehyde: dopamine, serotonin, tryptamine, 5-methoxytryptamine etc., to serum albumin. Only the serotonin derivative was active. The result shows that the discrimination specificity observed in immunohistochemistry is due to the paraformaldehyde fixation. It is concluded that for histochemical detection of serotonin by YC5/45, two reactive sites are necessary. The -CH2-CH2-NH2 group is probably modified by formaldehyde to produce a cyclic derivative to form the antibody recognition site. A different formaldehyde reactive site is required for cross linking to the tissue and this is provided by the presence of the 5-OH of serotonin which is absent in the others.

Animals↗
PubMed1979

Variations in mitochondrial monoamine oxidase during progressive starvation in the brain of developing rats.

Effects of progressive starvation of 12, 24, 48 and 60 h upon brain mitochondrial monoamine oxidase activity were studied. The enzyme activity was determined by three different substrates: 14C-labeled tryptamine, dopamine and kynuramine. With dopamine as substrate, the enzyme activity showed decline during 24 and 48 h of starvation. Monoamine oxidase when determined by tryptamine as the substrate, showed a decrease after 60 h of starvation. The use of kynuramine as substrate also produced a decrease in enzyme activity after 48 and 60 h of starvation. Refeeding the 60-h-starved rats for the following 24 h resulted in further decrease of monoamine oxidase activity of brain mitochondria from the 60 h starved values. The results suggest that oxidative deamination of biogenic amines is greatly inhibited during progressive starvation and remains low even after feeding the 60 h starved rats for 24 h.

Animals↗
PubMed1982

Effect of several biogenic amines on in vitro progesterone secretion by the bovine corpus luteum.

1. The effect of several biogenic amines on secretion of progesterone (P4) was examined using bovine corpora lutea (n = 6), removed on day 13 of the oestrus cycle, enzymatically dispersed and cultured in vitro. 2. Luteal cell cultures were co-incubated with 0, 10, 50 or 100 ng of luteinizing hormone (LH) and 50 ng of epinephrine (EPI), norepinephrine (NOR), dopamine (DOPA), melatonin (MEL), N-acetyl-50H-serotonin (N-acetyl-50H-tryptamine; NacS), serotonin (50H-tryptamine; 5HT) or saline control. 3. EPI, NOR and DOPA decreased baseline release of P4. 4. The magnitude of the response of P4 to LH was depressed when cells were co-incubated with DOPA, EPI and 5HT and stimulated when cells were co-incubated with MEL and NacS. 5. These data indicate that the biogenic amines might modulate ovarian steroidogenesis supplementary to hypothalamic-hypophyseal hormonal mechanisms.

Animals↗
PubMed1988

Biogenic amines and active peptides in the skin of fifty-two African amphibian species other than bufonids.

1. Extracts prepared from dried or fresh skins of 52 African amphibian species, other than bufonids, were subjected to chemical (colour reactions) and biological screening, to determine occurrence and contents of aromatic biogenic amines and peptides active on smooth muscle preparations and blood pressure. 2. Only indolealkylamines were detectable in the skins. They were represented by 5-hydroxytryptamine, its N-methylated derivatives and tryptamine. The indolealkylamines considered included the alkaloid trypargine, a carboline derivative resulting from the condensation of tryptamine with arginine. 3. The peptide families identified in skin extracts of the African frogs were as follows: caeruleins (caerulein, [Asn2, Leu5] caerulein), tachykinins (kassinin, [Glu2, Pro5] kassinin, hylambatin), bradykinins [( Hyp3] bradykinin), xenopsin, thyrotropin releasing hormone, peptide PYLa and the magainins I and II. The last five peptides have been so far identified only in the skin of Xenopus laevis, together with their precursors. 4. Since numerous other peptide molecules await isolation, elucidation of structure, and definition of possible biological activities, the array of peptides occurring in the skin of African amphibians, as in that of Australian and American amphibians, is destined to increase.

Amphibians↗
PubMed2006

The effects of non-medically used psychoactive drugs on monoamine neurotransmission in rat brain.

We developed a reproducible, simple, and small-scale method for determining the re-uptake and release of monoamines (dopamine, serotonin (5-HT) and norepinephrine) using rat brain synaptosomes. These assays were then applied to study the effects of different kinds of non-medically used psychoactive drugs on monoamine re-uptake and release. The phenethylamine derivatives, 4-fluoroamphetamine, 2-methylamino-3,4-methylene-dioxy-propiophenone (methylone), 1-(1,3-benzodioxol-5-yl)-2-butanamine (BDB), and N-methyl-1-(1,3-benzodioxol-5-yl)-2-butanamine (MBDB), had strong inhibitory effects on the re-uptake of dopamine, 5-HT and norepinephrine. 4-Fluoroamphetamine, methylone and BDB also strongly increased the release of the three monoamines, but MBDB increased 5-HT and norepinephrine release, but had little effect on dopamine release. However, 2,5-dimethoxy-4-iodophenethylamine (2C-I), 2,5-dimethoxy-4-ethylphenethylamine (2C-E), 2,5-dimethoxy-4-chlorophenethylamine (2C-C), 2,4,5-trimethoxyamphetamine (TMA-2) and 2,4,6-trimethoxyamphetamine (TMA-6), which are methoxylated phenethylamine derivatives, slightly influenced the re-uptake and release of monoamines. Alpha-metyltryptamine (AMT), a tryptamine derivative, was one of the strongest re-uptake inhibitors and releasers of the three monoamines. The tryptamine derivative, 5-methoxy-alpha-methyltryptamine (5-MeO-AMT), also strongly inhibited re-uptake and increased the release of the three monoamines. N,N-dipropyltryptamine (DPT), 5-methoxy-N,N-diisopropyltryptamine (5-MeO-DIPT), 5-methoxy-N,N-methylisopropyltryptamine (5-MeO-MIPT), and 5-methoxy-N,N-dimethyltryptamine (5-MeO-DMT) inhibited monoamine re-uptake, but had a few effects on monoamine release. 1-(3-Chlorophenyl)piperazine (3CPP) and 1-(methoxyphenyl)piperazine (4MPP), which are piperazine derivatives, inhibited monoamine re-uptake and accelerated their release. The results suggest that some designer drugs strongly act on the central nerve system to the same extent as restricted drugs.

Adrenergic Uptake Inhibitors↗
PubMed2005

Natural and directed biosynthesis of communesin alkaloids.

A role for tryptophan, acetate, mevalonate and methionine in the biosynthesis of communesins A and B, novel structurally-related and biologically-active Penicillium metabolites, has been established by isotopic labelling techniques. The incorporation of (14)C-tryptamine has also been demonstrated. dl-2-(13)C-tryptophan specifically enriched two carbon atoms in the (13)C NMR spectrum, thereby defining the intra-molecular arrangement of the two tryptophan-derived moieties. Feeding differentially labelled precursors during communesin production showed that tryptophan and methionine are involved early in the biosynthesis and that mevalonate provides an isoprene which is added later. A biosynthetic pathway involving an early precursor based on tryptophan is proposed. Indole-N-((13)C-methyl) tryptophan was not incorporated into communesins implying that N-methylation of tryptophan is not the first step of the communesin biosynthetic pathway. During deamination of indole-N-((13)C-methyl) tryptophan to 1-(13)C-methylindole-3-carboxylic acid communesin biosynthesis was inhibited. Of several halogenated indoles tested for directed biosynthesis, only dl-6-fluoro-tryptophan and 6-fluoro-tryptamine caused accumulation of the corresponding monofluoro-analogues of communesins A and B.

Alkaloids↗
PubMed2003

Characterization of the 5-HT6 receptor coupled to Ca2+ signaling using an enabling chimeric G-protein.

We examined the feasibility of coupling the 5-HT(6) receptor to a Ca(2+) signaling read-out using a chimeric G-protein, comprising of G(alphaq) with the C-terminal five amino acids from G(alphas), to facilitate assays on the fluorometric imaging plate reader (FLIPR). Using a transient transfection assay in human embryonic kidney (HEK) cells, Ca(2+) signaling in response to serotonin (5-HT) was facilitated by co-transfection of the 5-HT(6) receptor with the G(alphaq)/G(alphas) chimera, but not with the 5-HT(6) receptor alone or with a similar chimera incorporating the C-terminal five amino acids of G(alphai3). A series of agonist concentration-response curves were constructed using the 5-HT(6)-G(alphaq)/G(alphas) signaling assay generating the following rank order of agonist potency; 5-methoxytryptamine (EC(50), 9 nM)=5-HT (12 nM)=2-methyl 5-HT (13 nM)>tryptamine (86 nM)=5-carboxamidotryptamine (5-CT) (119 nM)>>lisuride (>1 microM). In comparison, essentially identical EC(50) values were observed for the stimulation of cAMP accumulation with the same compounds; 5-methoxytryptamine (EC(50), 6 nM)=5-HT (6 nM)=2-methyl 5-HT (15 nM)>tryptamine (91 nM)=5-CT (153 nM)>lisuride (>350 nM). Clozapine and SB 271046 both produced a concentration-dependent antagonism of the 5-HT-stimulated Ca(2+) response with IC(50) values of 45 and 11 nM, respectively. In contrast, aripiprazole, a recently launched atypical anti-psychotic with a novel mechanism of action described as a dopamine/serotonin stabilizer, was essentially devoid of 5-HT(6) receptor antagonist activity. Our results demonstrate that a FLIPR-based Ca(2+) signaling assay is a feasible approach to the functional characterization of 5-HT(6) receptor ligands. Moreover, the equivalent coupling efficiency, as indexed by agonist potency, observed using this system compared with the native coupling assay to cAMP suggests that the C-terminal five amino acids of G(alphas) are the major determinant for the receptor/G-protein interaction of the 5-HT(6) receptor subtype.

Calcium↗
PubMed1998

The human 5-ht5A receptor couples to Gi/Go proteins and inhibits adenylate cyclase in HEK 293 cells.

The G protein coupling of human 5-hydroxytryptamine5A (h5-ht5A) receptors was investigated in stably transfected human embryonic kidney (HEK) 293 cells, using radioligand and guanosine-5'[gamma-35S]thiotriphosphate binding to membranes and cyclic adenosine monophosphate measurements in cells. 5-Carboxamido[3H]tryptamine bound to high- and low-affinity sites on h5-ht5A-HEK 293 cell membranes. Guanylyl-imidodiphosphate addition and pertussis toxin pre-treatment abolished high-affinity binding, indicating coupling to G proteins of the Gi/Go family. [N-methyl-3H]Lysergic acid diethylamide bound to a single site; guanylyl-imidodiphosphate and pertussis toxin did not alter lysergic acid diethylamide affinity. 5-Hydroxytryptamine stimulated guanosine-5'[gamma-35S]thiotriphosphate binding to 130% over basal and this effect was completely abolished by pertussis toxin. Various 5-hydroxytryptamine receptor ligands were tested for inhibition of 5-carboxamido[3H]tryptamine binding and in guanosine-5'[gamma-35S]thiotriphosphate binding assays. 5-Hydroxytryptamine consistently inhibited forskolin-induced cyclic adenosine monophosphate formation by 25% in h5-ht5A-HEK 293 cells; no effect was detected on basal cyclic adenosine monophosphate levels, on intracellular Ca2+ concentration or arachidonic acid release. Our studies demonstrate functional coupling of the h5-ht5A receptor to pertussis toxin-sensitive G proteins and to inhibition of adenylate cyclase activity.

Adenylate Cyclase Toxin↗
PubMed2002

Screening of Catharanthus roseus secondary metabolites by high-performance liquid chromatography.

Two direct HPLC analytical methods for the screening of the major indole alkaloids of Catharanthus roseus hairy roots and their iridoid precursors have been developed. Photodiode array and fluorescence detection were performed. The separation was achieved on a reversed-phase C18 column. The first method allowed the separation of catharanthine, serpentine, tabersonine, vindoline, vinblastine, and vincristine in 20 min. Ajmalicine, tryptophan, tryptamine and secologanine were separated using the second method in 13 min. The identification of the compounds was based on the retention time and the comparison of UV spectra with those of authentic standards. A simplified alkaloid extraction method was developed in order to accelerate sample preparation. The assays were successfully used to quantify major compounds of the secondary metabolism of hairy root cultures of C. roseus, thus providing a reliable tool for rapid screening of C. roseus secondary metabolite samples. In these cultures, ajmalicine, serpentine, catharanthine, tabersonine, and tryptamine were detected, but tryptophan, vindoline, vinblastine and vincristine were not.

Catharanthus↗
PubMed2002

1-(Benzofuran-2-yl)-2-(3,3,3-trifluoropropyl)aminopentane HCl, 3-F-BPAP, antagonizes the enhancer effect of (-)-BPAP in the shuttle box and leaves the effect of (-)-deprenyl unchanged.

The subcutaneous administration of 1 mg/kg tetrabenazine, once daily for 5 days, which depletes the catecholamine stores in the brain, significantly inhibits in rats the acquisition of a two-way conditioned avoidance reflex in the shuttle box. Enhancer substances, the tryptamine-derived selective and highly potent enhancer, R-(-)-1-(benzofuran-2-yl)-2-propylaminopentane HCl [(-)-BPAP] (0.05-10 mg/kg), the beta-phenylethylamine (PEA)-derived enhancer, (-)-deprenyl (1-5 mg/kg) and the (-)-deprenyl analogue, free of MAO-B inhibitory potency, (-)-1-phenyl-2-propylaminopentane HCl [(-)-PPAP], (1-5 mg/kg), antagonize in a dose-dependent manner the inhibition of learning caused by tetrabenazine. 1-(Benzofuran 2 yl)-2-(3,3,3-trifluoropropyl)aminopentane HCl [3 F BPAP], a newly synthetized analogue of (-)-BPAP with low specific activity, significantly antagonized the enhancer effect of (-)-BPAP but left the effect of (-)-deprenyl and (-)-PPAP unchanged. This is the first proof for a difference in the mechanism of action between a PEA-derived enhancer substance and its tryptamine-derived peer.

Adrenergic Uptake Inhibitors↗
PubMed2002

The biosynthesis of beta-carboline and quinolizidine alkaloids of Alangium lamarckii.

The incorporation of tryptamine, dopamine, N-deacetylisoipecoside, N-deacetylipecoside into alangimarckine, deoxytubulosine and ankorine and of strictosidine and vincoside into alangimarckine and deoxytubulosine in young Alangium lamarckii Thw. (Alangiaceae) has been studied and specific utilisation of N-deacetylisoipecoside demonstrated. Parallel experiments with nordeoxytubulosine and deoxytubulosine suggested that O-methylation precedes condensation of protoemetine with tryptamine and further the reduction of ethylene side chain takes place before condensation. Hydroxylation at C-8 in the trans-quinolizidine moiety is the terminal step in the biosynthesis of alangimarckine.

Alangiaceae↗
PubMed1997

Role of dopamine in behavioral effects of serotonin microinjected into rat striatum.

Bilateral local microinfusion of serotonin (5-hydroxytryptamine; 5-HT) into the ventrolateral striatum (VLS) of the rat forebrain induces quantifiable stereotyped orofacial behaviors. The role of presynaptic dopamine (DA) and structural requirements of indoles for expression of this behavioral effect and for inhibition of neuronal transport of [3H]DA were examined. Bilateral local injection of 6-OHDA (8 micrograms/side) into VLS depleted DA and markedly diminished the behavioral effects of 5-HT. Intracerebral pretreatment with the potent DA transport inhibitors GBR-12909 (6 micrograms/side) or nomifensine (4 micrograms/side) also markedly decreased behavioral responses to 5-HT. A series of indoles and tyramine were examined for ability to induce stereotypy following infusion into the VLS. Of compounds tested, only p-tyramine, 5-HT, tryptamine and L-5-hydroxytryptophan (5-HTP) elicited strong orofacial behaviors; indoles lacking a free amino group or containing other substituents were virtually inactive in vivo, and the effect of 5-HTP was prevented by systemic pretreatment with the decarboxylase inhibitor NSD-1015, indicating its required conversion to 5-HT. Uptake of [3H]DA (0.1 microM) into rat striatal synaptosomes was inhibited in a concentration-dependent manner in the following apparent rank-order: p-tyramine, N-methyl-5-HT, tryptamine, 5-HT, N-methyltryptamine (IC50 = 44-718 nM), other indoles (IC50 = 10-100 microM). These results support the conclusion that oral stereotypy induced by microinjection of 5-HT or other aromatic amines into rat VLS is mediated by local release of endogenous DA. These results extend previous findings indicating that this effect of 5-HT was not blocked by 5-HT receptor antagonists, and suggest mediation by a neuronal transport process involved in the uptake or storage of DA.

Animals↗