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At least 19 recordsLinked to original sources

PubMed1983

The biosynthesis of p-tyramine, m-tyramine, and beta-phenylethylamine by rat striatal slices.

Slices of striatal tissue obtained from saline-injected rats were incubated with 3H-phenylalanine in the presence of pargyline. This resulted in the formation of 3H-m-tyramine, 3H-p-tyramine, and 3H-phenylethylamine. Pretreatment of the rats with alpha-methyl-p-tyrosine reduced the formation of 3H-m-tyramine and 3H-p-tyramine, but enhanced the formation of 3H-phenylethylamine. After incubation of striatal tissue obtained from saline-injected rats with 3H-ptyrosine, only 3H-p-tyramine was produced. In this case, alpha-methyl-p-tyrosine pretreatment enhanced 3H-p-tyramine formation. Striatal slices incubated with 3H-m-tyramine or 3H-p-tyramine did not yield any significant quantity of 3H-phenylethylamine; nor was 14C-phenylethylamine converted to 14C-m-tyramine or 14C-p-tyramine. Pretreatment of the rats with the monoamine oxidase inhibitor pargyline did not appreciably affect these findings. After incubation with 3H-dopamine very small quantities of 3H-m-tyramine and 3H-p-tyramine were formed, the ratio between them being 7:1. It is concluded that the major biosynthetic route for m-tyramine formation in the rat striatum is by hydroxylation of phenylalanine, probably by tyrosine hydroxylase to m-tyrosine, followed by decarboxylation, probably by L-aromatic amino acid decarboxylase, to m-tyramine. para-Tyramine is formed by decarboxylation of p-tyrosine, and phenylethylamine similarly by decarboxylation of phenylalanine.

Animals↗

PubMed1983

The effects of (+)-amphetamine, alpha-methyltyrosine, and alpha-methylphenylalanine on the concentrations of m-tyramine and alpha-methyl-m-tyramine in rat striatum.

The concentration in rat striatum of the meta and para isomers of tyramine and alpha-methyltyramine, after the administration of (+)-amphetamine, alpha-methyl-p-tyrosine (AMPT) and alpha-methylphenylalanine (AMPA) has been determined using chemical ionization gas chromatography mass spectrometry (c.i.g.c.m.s.). Twenty hours after the last of 7 daily injections of (+)-amphetamine (5 mg kg-1 i.p.) the concentration of alpha-methyl-p-tyramine in striatal tissue increased twofold compared to the concentration 20 h after a single injection. In contrast the concentration of alpha-methyl-m-tyramine did not change. alpha-Methyl-m-tyramine and alpha-methyldopamine were found in the striatum at concentrations of 42 ng g-1 and 13.5 ng g-1 respectively after treatment of rats 20 h before with AMPA (100 mg kg-1 i.p.). After treatment with AMPT (100 mg kg-1, 20 h before decapitation) only the para isomer of alpha-methyltyramine could be detected (13.7 ng g-1) although the striatal concentration of alpha-methyldopamine was 274 ng g-1, a level 20 times greater than that observed after AMPA treatment. The combined administration of both AMPT and AMPA (100 mg kg-1 each, 20 h) resulted in a reduction of the striatal concentration of alpha-methyl-m-tyramine but not alpha-methyl-p-tyramine. These data suggest that alpha-methyl-m-tyramine in rat striatum is formed by the enzyme tyrosine hydroxylase on substrate AMPA, rather than by ring dehydroxylation of alpha-methyldopa and alpha-methyldopamine. Significant reductions in the striatal concentrations of m-tyramine 2 h after the administration of AMPT, suggest that tyrosine hydroxylase is involved similarly in the production of m-tyramine.

Amphetamine↗

PubMed1984

The effects of administration of meta-tyramine and para-tyramine on dopamine and its metabolites in the rat striatum.

Para-tyramine administration decreased the release of dopamine as indicated by the decline in 3-MT concentrations, increased HVA concentrations at 30 and 60 min and decreased DA concentrations at the same times. DOPAC concentrations declined after 60 min. Meta-tyramine reduced the synthesis of dopamine thus causing a decrease in the concentrations of all its metabolites by 60 min post injection. The failure of the deaminated products of the tyramines to affect the concentrations of dopamine and its metabolites suggested that the effects produced by either meta or para-tyramine were due to the amines and not due to interference with various transport mechanisms. Para-tyramine and meta-tyramine may achieve their actions on dopamine neurotransmission by different mechanisms. Para-tyramine may act as a partial agonist reducing DA release extraneuronally (the decrease in 3-MT levels) or by displacing DA intraneuronally as evidenced by the decline in DA concentrations or increase in HVA concentrations. Meta-tyramine appears to inhibit the synthesis of dopamine.

3,4-Dihydroxyphenylacetic Acid↗

PubMed2004

(-)-Deprenyl inhibits tyramine-induced noradrenaline release, but not tyramine-induced dopamine release or potassium-induced noradrenaline release, from rat brain synaptosomes.

The effect of (-)-deprenyl (selegiline), a therapeutic agent for Parkinson's disease, on the tyramine-induced release of catecholamine from rat brain synaptosomes was studied using a superfusion system. Tyramine (10(-7) to 10(-5)M) enhanced the release of [3H]noradrenaline (NA) and [3H]dopamine (DA) from forebrain and striatal synaptosomes in a dose-dependent manner. (-)-Deprenyl (5x10(-5)M) had no effect on spontaneous catecholamine release, suggesting that it has no tyramine-like catecholamine releasing effect. Pretreatment with (-)- or (+)-deprenyl (5x10(-5)M) significantly prevented the tyramine (10(-6)M)-induced NA release, but not DA release. The inhibitory action of (-)-deprenyl was not observed on potassium (15mM)-induced NA release. (-)-Desmethyldeprenyl (5x10(-5)M), a metabolite of (-)-deprenyl, and a monoamine oxidase-A (MAO-A) inhibitor, clorgyline (5x10(-5)M), failed to block the tyramine-induced NA and DA release. Although (+)-deprenyl, a potent DA uptake inhibitor, did not inhibit tyramine-induced DA release, a catecholamine uptake inhibitor nomifensine (5x10(-5)M) did. In summary, (-)-deprenyl at a dose inhibiting tyramine-induced NA release did not have any effect on tyramine-induced DA release or potassium-induced NA release.

Animals↗

PubMed1981

Release of radiolabeled dopamine, p-tyramine, and m-tyramine from rat striatal slices by some aminotetralins.

The effect of several 2-aminotetralins (2ATs) on the uptake and release of [14C] dopamine and [2H]m- or [3H]p-tyramine by rat striatal slices was examined. 6,7-Dihydroxy-2AT (6,7OHAT) and 5,6-dihydroxy-2-methyl-AT (5,6OHMeAT) were the most potent uptake inhibitors as well as the most potent releasers of the three labeled amines. The 5-, 6-, and 7-hydroxy-2-N, N-dipropyl-ATs (5-, 6-, and 7OHdiPrAT) and 5,6-dihydroxy-2-N,N-dipropyl-AT (5,6OHdiPrAT) significantly inhibited the uptakes of the three labeled amines, but they released only the tyramines. The dipropyl substitutions of a 2AT appeared to confer a tyraminergic specificity to its release properties. To verify this supposition, 2AT was compared to 2-N,N-dipropyl-AT (diPrAT). Although 2AT released both [3H]p-tyramine and [14C]dopamine, diPrAT released only [3H]p-tyramine. None of the compounds, however, differentiated between m- and p-tyramine. It was concluded that the release of tyramines could be implicated in the actions of some of the 2ATs and that the tyramines can be transported independently from dopamine.

2-Naphthylamine↗

PubMed1977

Urinary p-tyramine in hereditary tyrosinemia: II. Origin of urinary p-tyramine.

1. A patient with hereditary tyrosinemia (tyrosinosis) was given oral loads of p-tyramine and tyrosine with and without medication (neomycin) to investigate the respective roles of intestinal bacteria and tissues in accounting for the origin of urinary p-tyramine. 2. The excretion of a high circulating level of p-tyramine following an oral load of p-tyramine in a patient with hereditary tyrosinemia (tyrosinosis) was as conjugated p-hydroxyphenylacetic acid (p-HPAA) and conjugated p-tyramine. 3. Both intestinal bacterial activity and tissue decarboxylation appeared to account for urinary p-tyramine in this patient following an oral load of tyrosine. 4. Sterilization of the gut by oral neomycin and a second load of oral tyrosine further supported a predominate role for tissue decarboxylation in the origin of urinary p-tyramine. 5. The data suggested that a major route of tyrosine metabolism in man may be via tissue decarboxylation of tyrosine.

4-Hydroxyphenylpyruvate Dioxygenase↗

PubMed1992

Block of sodium channels by tyramine and its analogue (N-feruloyl tyramine) in frog ventricular myocytes.

Pharmacological effects of tyramine and its analogue, N-feruloyl tyramine (NFT), on sodium and calcium currents in frog ventricular myocytes were examined using the whole-cell voltage-clamp technique. To improve the temporal and spatial control of the membrane potential, sodium currents (INa) were recorded in 45.5 mM [Na+]o at 10 degrees C. Both tyramine and NFT (1-100 microM) induced a concentration-dependent decrease in INa evoked from a holding potential of -80 mV without affecting a change in either the time to peak or the time constant for the falling phase of INa. Similarly the reversal potential for INa remained unchanged at a value close to that predicted from the Nernst equation. The finding that both tyramine and NFT decreased INa when activated maximally, from a holding potential of -120 mV, indicates that the amplitude of INa can be reduced independently of a change in the kinetics of the current. In addition, tyramine (100 microM) shifted the membrane potential for half maximal inactivation (Vh) of the steady-state inactivation (h infinity)-curve from -74 to -84 mV without affecting its slope. In contrast, NFT failed to affect the h infinity-curve. The calcium current (ICa) recorded in the presence of 0.3 microM TTX was not affected by either 100 microM tyramine or NFT. We concluded that tyramine directly blocks Na channel by shifting h infinity-curve and by suppressing maximum Na channel conductance, while NFT suppresses only maximum Na channel conductance.

Animals↗

PubMed1979

Uptake of para-tyramine and meta-tyramine into slices of the caudate nucleus and hypothalamus of the rat.

The kinetics of the uptake of p-tyramine, m-tyramine, and dopamine were investigated in slices of the hypothalamus and striatum of the rat in the presence of nialamide. When uptake was analyzed by a least-squares fit to a Lineweaver-Burk plot, each amine appeared to be concentrated by both a "low"-affinity and a "high"-affinity system in both brain regions. The obtained Km and Vmax values for the "high"-affinity uptake system for each amine in both brain regions were similar. In general terms, the uptake systems in the striatum exhibited larger Km and Vmax values, with the velocity of uptake being in the order dopamine less than m-tyramine less than p-tyramine. 2,4-Dinitrophenol (DNP) and ouabain reduced all uptakes in the caudate, but reduced only the "high"-affinity uptake of m-tyramine and the "low"-affinity uptake of dopamine in the hypothalamus.

Animals↗

PubMed1998

Tyramine-amplified immunohistochemical testing using "homemade" biotinylated tyramine is highly sensitive and cost-effective.

Immunohistochemical testing using biotinylated tyramine is a recently described technique that results in a strong amplification of the detection signal using antibodies at very high dilutions. In this report we compare the sensitivity and cost-effectiveness of the technique using "homemade" biotinylated tyramine with those of two commercially available kits. The technique using homemade tyramine was easy to follow and highly sensitive and resulted in a 2.5- to 5-fold reduction in costs compared with the commercial kits. Tyramine-amplified immunohistochemical testing using homemade biotinylated tyramine is a valuable and inexpensive tool for both the diagnostic and experimental histopathology laboratory.

Biotinylation↗

PubMed1980

The inhibition of tyramine oxidation and the tyramine hypertensive response ("cheese effect") may be independent phenomena.

Although the selective monoamine oxidase (MAO) inhibitor, (-)-deprenyl, substantially inhibits tyramine-oxidizing ability in the pig, intravenous tyramine challenge after pretreatment with this drug failed to produce the characteristic pressor response ("cheese effect") associated with other irreversible MAO inhibitors. Conversely, pretreatment with the tyramine oxidation-sparing selective MAO inhibitor, clorgyline, followed by intravenous tyramine, paradoxically resulted in a profound pressor response. We suggest that the action of standard MAO-inhibiting drugs may be compounded of two separate actions, usually associated but, in fact, unreleated.

Animals↗

PubMed2005

Elevated tyrosine decarboxylase and tyramine hydroxycinnamoyltransferase levels increase wound-induced tyramine-derived hydroxycinnamic acid amide accumulation in transgenic tobacco leaves.

Feruloyltyramine (FT) and 4-coumaroyltyramine (4CT) participate in the defense of plants against pathogens through their extracellular peroxidative polymerization, which is thought to reduce cell wall digestibility. Hydroxycinnamoyl-CoA:tyramine N-(hydroxycinnamoyl)transferase (THT; EC 2.3.1.110) and tyrosine decarboxylase (TYDC; EC 4.1.1.25) are purported to play key roles in the stress-induced regulation of tyramine-derived hydroxycinnamic acid amide (HCAAT) metabolism. Transgenic tobacco (Nicotiana tabacum cv. Xanthi) was engineered to constitutively express tobacco THT. A T1 plant over-expressing THT was crossbred with T1 tobacco expressing opium poppy TYDC2, to produce a T2 line with elevated THT and TYDC activities compared with wild type plants. The effects of an independent increase in TYDC or THT activity, or a dual increase in both TYDC and THT on the cellular pools of HCAAT pathway intermediates and the accumulation of soluble and cell wall-bound FT and 4CT were examined. Increased TYDC activity resulted in a larger cellular pool of tyramine and lower levels of L-phenylalanine in transgenic leaves. In contrast, elevated THT activity reduced tyramine levels. HCAAT levels were low in healthy leaves, but were induced in response to wounding and accumulated around wound sites. Similarly, endogenous THT and TYDC activities were wound-induced. The rate of wound-induced HCAAT accumulation was highest in transgenic plants with elevated THT and TYDC activities showing that both enzymes exert control over the flux of intermediates involved in HCAAT biosynthesis under some conditions.

Acyltransferases↗

PubMed1987

The regional distribution of p-tyramine and m-tyramine in the rat corpus striatum and the effect of monoamine oxidase inhibition.

These experiments show that in the rat corpus striatum the highest concentrations of p- and m-tyramine were found in the caudate nucleus while somewhat lower values were observed in the putamen and globus pallidus. Inhibition of monoamine oxidase by pargyline produced an increase in the concentration of both tyramines in the three areas. The effect of pargyline is more marked with p-tyramine, however, the regional distribution of both p- and m-tyramine are preserved after monoamine oxidase inhibition. In addition, the pargyline treatment produced a significant reduction in corpus striatum p-tyrosine while no changes were observed in the tryptophan concentrations.

Animals↗

PubMed1980

Interactions between p-tyramine, m-tyramine, or beta-phenylethylamine and dopamine on single neurones in the cortex and caudate nucleus of the rat.

p-Tyramine, applied to cortical and caudate neurones with weak iontophoretic currents (0-10 nA), did not usually cause any alteration of base-line firing rate. However, neuronal responses to dopamine (DA) during such weak applications of p-tyramine were greatly enhanced. Cortical neurone responses to noradrenaline (NA) were similarly potentiated, but both cortical and caudate neurone responses to alpha-aminobutyric acid were unaffected by p-tyramine. In addition, weak background applications of DA which did not affect cell firing rate were also without effect on the neuronal responses to the standard application of DA. The responses of cortical neurones to DA were also potentiated by m-tyramine and beta-phenylethylamine applied with weak cationic currents. The results may suggest that trace amines can enhance NA and DA transmission in the central nervous system.

Action Potentials↗

PubMed1995

N' alkylamine low molecular mass heparins (LMM-heparin-tyramine and LMM-heparin-tyramine-fitc) exhibit long lasting anticoagulant effects.

The pharmacodynamic and pharmacokinetic properties of endpoint-attached N'alkylamine derivatives of low molecular mass heparin (LMMH), low molecular mass heparin (LMMH), low molecular mass heparin-tyramine (LMMH-tyr) and low molecular mass heparin-tyramine-fluorescein-5-isothiocyanate (LMMH-tyr-fitc) were investigated ex vivo. After intravenous bolus injection of LMMH, LMMH-tyr and LMMH-tyr-fitc (150 aXa U/kg) to Sprague-Dawley rats (n = 8), LMMH-tyr and LMMH-tyr-fitc displayed decreased clearances. The beta-half-life time of the antifactor Xa (aXa) of "endpoint-attached heparins" was significantly prolonged: LMMH-tyr (125 min), LMMH-tyr-fitc (141 min) compared to LMMH (69 min). The pharmacokinetics of LMMH-tyr-fitc were measured with reversed phase high performance liquid chromatography (RP-HPLC). It showed a decreased clearance and a prolonged half-life time (132 min). The selectively tagged LMMH-tyramine and LMMH-tyramine-fitc may be used to investigate the pharmacokinetics, plasma protein and cellular binding of low molecular mass heparins.

Animals↗

PubMed1978

Uptake and release of meta-tyramine, para-tyramine, and dopamine in rat striatal slices.

The uptakes of high-affinity concentrations (10(-8)M) of meta-tyramine (m-TA), para-tyramine (p-TA), and dopamine (DA) into rat striatal slices have been shown to be inhibited by DNP and ouabain. We now demonstrate that cocaine (5 x 10(-6)M) and low concentrations of sodium ion (26 x 10(-3)M) also reduced these uptakes. The spontaneous efflux and the release [induced by an elevated concentration of potassium ion (5 x 10(-2)M)] of each of the previously accumulated amines were studied in the presence and absence of added calcium ions. The spontaneous efflux of each amine (especially the tyramines) was enhanced by the absence of calcium ions. Part of this enhancement seemed to be due to an inhibition of a calcium-dependent reuptake. The elevated concentration of potassium ion proved to be an effective releaser of each amine; and for DA, such release was decreased by the removal of calcium. For m- and p-TA, however, the removal of calcium either did not reduce or completely abolished the releases depending upon the duration of the calcium removal. The significance of these findings is discussed.

Animals↗

PubMed1991

Deuterium-labelled p-tyramine challenge test and phenolsulfotransferase activity in depressed patients--failure to replicate decreased p-tyramine conjugation in depression.

1. Depressed and normal subjects were challenged with deuterium-labelled p-tyramine and urine was collected for 3 h. 2. Urinary excretion of conjugated p-tyramine was not significantly different between normal, melancholic and non-melancholic depressed subjects. 3. Platelet phenolsulfotransferase activity to p-tyramine (p less than 0.05) and to phenol (p less than 0.005) were significantly lower in the depressed patients.

Amitriptyline↗

PubMed1974

The effect of oral inorganic sulphate on the metabolism of 4-hydroxyphenethylamine (tyramine) in man: tyramine O-sulphate measurement in human urine.

1. Urinary excretion of tyramine O-sulphate in six normal human subjects after an oral dose of 125mg of tyramine hydrochloride alone, and with a supplement of Na(2)SO(4), was determined by using chromatographic and electrophoretic separations followed by spectrophotofluorimetry. 2. In every case the excretion of tyramine O-sulphate was increased significantly after sulphate supplementation.

Carbon Radioisotopes↗

PubMed1978

Evidence for the presence of m-tyramine, p-tyramine, tryptamine, and phenylethylamine in the rat brain and several areas of the human brain.

Postmortem human brains have been obtained from four nonpsychiatric patients, aged 59-70 years. Regional analysis of the trace amines phenylethylamine, p-tyramine, m-tyramine, and tryptamine has indicated that the amines are distributed heterogeneously throughout the brain, but are most concentrated in the basal ganglia. Although the levels are very low, evidence obtained from animal studies has indicated that the trace amines have a very rapid turnover rate. Their presence in a brain synaptosomal fraction suggests a possible involvement in the process of neurotransmission. Postmortem changes in human brain amines are discussed in relation to those occurring postmortem in the rat brain, in which phenylethylamine, p-tyramine, and tryptamine have been shown to increase to levels greater than those prevailing in vivo.

Aged↗