SEARCH · PubMed Health

Results for “TYRAMINE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 127 records · Page 7Linked to original sources

PubMed1996

Failure of tyramine to release neuronal ATP as a cotransmitter of noradrenaline in the guinea-pig vas deferens.

Contractions, release of noradrenaline and release of ATP elicited by the indirectly acting sympathomimetic amine tyramine and responses elicited by exogenous noradrenaline were studied in the isolated vas deferens of the guinea pig. Release of noradrenaline was assessed as overflow of tritium after preincubation with [3H]-noradrenaline. ATP was measured by means of the luciferin-luciferase technique. In tissues pretreated with pargyline 1 mM, tyramine 300 microM, when added to the superfusion medium for 2 min, elicited contraction and an overflow of tritium (mainly [3H]-noradrenaline) and ATP. Contraction and ATP overflow responses were prevented and tritium overflow was greatly reduced by desipramine 10 microM. Prazosin 0.3 microM abolished contractions and evoked ATP overflow without changing tritium overflow. Blockade of postjunctional P2-purinoceptors by suramin 300 microM caused a marked decrease of tyramine-evoked contractions and a slight reduction of tritium overflow whereas evoked ATP overflow was markedly increased. The effect on contraction was not shared by two other P2-purinoceptor antagonists, namely pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid (PPADS) 32 microM and diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS) 32 microM: PPADS increased contractions about fourfold, whilst DIDS had no effect at all. When the vas deferens was superfused for 24 min with medium containing tyramine 300 microM, evoked contractions and tritium overflow continued throughout whereas ATP overflow faded rapidly to basal values. In the presence of prazosin 0.3 microM, tyramine 300 microM again failed to elicit contractions as well as an overflow of ATP. Application of noradrenaline 10 microM instead of tyramine also resulted in prolonged contraction and an overflow of ATP that declined rapidly. It is concluded that all ATP released by tyramine is non-neuronal in origin, secondary to the activation of postjunctional alpha 1-adrenoceptors by released noradrenaline. The non-neural ATP does not seem to play a functional role in smooth muscle contraction and derives from a postjunctional source which is subject to a rapid depletion upon sustained alpha 1-adrenoceptor activation.

Adenosine Triphosphate↗

PubMed1991

Isolation of mono- and di-iodine 125 tyramines for conjugation labelling.

Here we describe a method for isolating mono- and di-iodine 125 tyramines from a crude tyramine radio-iodination reaction mixture. Tyramine was radio-iodinated according to a modified chloramine-T method. Mono- and diforms were separated from each other, as well as from free 125I and unreacted tyramine, by means of paper electrophoresis or thin-layer chromatography. Both 125I-tyramine derivatives finally obtained were pure and had high specific activities, which averaged 2500 Ci/mmol for mono-125I-tyramine and 5000 Ci/mmol for di-125I-tyramine. Due to their characteristics, these derivatives can be used for labelling various substances indirectly and preparing in vivo and in vitro tracers of high purity and specific activity, when conjugation labelling is required.

Iodine Radioisotopes↗

PubMed1983

The influence of adrenergic receptor antagonists on the amnestic and antiamnestic actions of adrenaline and tyramine.

The posttraining IP administration of adrenaline (epinephrine) HCl (5.0 micrograms/kg) or tyramine HCl (1.0 mg/kg) causes retrograde amnesia for a one-way step-down inhibitory avoidance task in rats. The effect is cancelled by the simultaneous injection of the alpha 2-adrenergic receptor antagonist yohimbine HCl (2.0 mg/kg) or of the beta 1 - beta 2 blocker propranolol HCl (2.0 mg/kg). The amnestic effect of posttraining adrenaline or tyramine is counteracted by the administration of adrenaline or tyramine prior to testing: each drug has a greater antiamnestic effect against itself than against the other drug. The antiamnestic effect of tyramine and adrenaline is antagonized by the simultaneous administration of prazosin or yohimbine, but not by that of propranolol. We conclude that the posttraining amnestic effect of adrenaline and tyramine is mediated by alpha 2 receptors (probably postsynaptic) and that it does not reflect a storage deficit, since memory can be restored by an appropriate treatment given before the test session. The antiamnestic effect of adrenaline and tyramine is mediated both by alpha 1 and by alpha 2 receptors, and probably reflects the dependency of mechanisms that make stored information available for retrieval on circulating catecholamines. The present findings provide no clue as to the anatomical distribution of the adrenergic receptors involved in the amnestic or antiamnestic actions of adrenaline and tyramine.

Adrenergic alpha-Antagonists↗

PubMed1981

Tyramine infusions and selective monoamine oxidase inhibitor treatment. I. Changes in pressor sensitivity.

The enhanced sensitivity to the pressor effects of tyramine, an indirect-aging sympathomimetic found abundantly in the diet, is a well-known potentially dangerous side effect occurring during treatment with commonly used non-selective monoamine oxidase (MAO) inhibitors. The effects of treatment with the selective MAO-A inhibitor clorgyline and the partially selective MAO-B inhibitors pargyline and deprenyl on tyramine's pressor effects were studied in depressed patients using an IV steady-state tyramine infusion technique. After 4 weeks of treatment, clorgyline produced a significantly greater increase in tyramine sensitivity in comparison to a medication-free baseline (29-fold) than did pargyline (12-fold) or deprenyl (1.7-fold). The pressor effects of tyramine were significantly prolonged after cessation of infusion during both clorgyline and pargyline, but not deprenyl treatment. These data from IV tyramine administrations suggest that intestinal MAO inhibition is not the major determinant of the enhanced tyramine pressor sensitivity produced by clorgyline and pargyline.

Blood Pressure↗

PubMed1991

Conversion of p-tyrosine to p-tyramine in the isolated perfused rat kidney: modulation by perfusate concentrations of p-tyrosine.

We used the isolated perfused rat kidney to evaluate the role of renal decarboxylation of p-tyrosine as the source of urinary p-tyramine. Kidneys were perfused with concentrations of p-tyrosine ranging from 0.02 mM to 2.0 mM. p-Tyramine was measured by a sensitive and specific radioenzymatic assay. An increase in the perfusate concentration of p-tyrosine resulted in a significant increase in p-tyramine production that was blocked by the addition of NSD-1015, an inhibitor of aromatic-1-amino decarboxylase (AADC). We conclude p-tyrosine is the precursor for the renal production of p-tyramine, renal AADC catalyzes the formation of urinary p-tyramine, synthesized p-tyramine is predominantly excreted in the urine, and p-tyramine synthesis is modulated by the arterial delivery of p-tyrosine to the kidney.

Animals↗

PubMed1984

Antisera against catecholamines: specificity studies and physicochemical data for anti-dopamine and anti-p-tyramine antibodies.

Antibodies against dopamine and p-tyramine were raised in rabbits. The two catecholamines were conjugated to albumin by glutaraldehyde. The specificity of the antibodies was established by equilibrium dialysis competition experiments using an immunoreactive tritiated derivative synthesized by coupling dopamine or p-tyramine to N-alpha-acetyl-L-lysine N-methylamide with glutaraldehyde. Hence, these radiolabelled ligands mimicked the antigenic determinant of conjugated immunogens. A comparison of the data obtained showed the high specificity of each antiserum for its hapten coupled by glutaraldehyde. The anti-dopamine antibodies recognized dopamine-glutaraldehyde but not p-tyramine-glutaraldehyde. The opposite occurred for the anti-p-tyramine antibodies. A slight modification of the molecular structure provided the opportunity for a specific response against that molecule. But this difference was more important when related to the hapten region where the antibody affinity was maximal. The cross-reactivity was observed to be more important dopamine and p-tyramine than between dopamine and noradrenaline on the one hand and between p-tyramine and dopamine than p-tyramine and octopamine on the other hand.

Animals↗

PubMed1994

In vitro release of [3H]noradrenaline by tyramine from the superior cervical ganglion and in the nictitating membrane of the cat.

1. The release and the metabolism of [3H]noradrenaline ([3H]NA) induced by tyramine was studied in the superior cervical ganglion (cell bodies) and in the nictitating membrane (nerve endings) of the cat. 2. Exposure of the ganglia to 58.0 and 174.0 microM tyramine resulted in the release of 13.7 and 11.8% respectively of the total tissue radioactivity. In the nictitating membrane, the fractional release of radioactivity was directly proportional to the concentration of tyramine (5.8, 58.0 and 174.0 microM). 3. In ganglia [3H]DOPEG accounted for 55.8% of the radioactivity released by 58.0 microM tyramine and only 10.5% of the radioactivity was unmetabolized NA. In presence of 174.0 microM tyramine, [3H]NA increased to 28.0% of the total radioactivity and [3H]DOPEG and [3H]OMDA decreased to 45.3 and 18.9% respectively. 4. In the nerve endings, the contribution of [3H]NA, [3H]DOMA and [3H]NMN increased with the concentration of tyramine while [3H]DOPEG decreased. 5. The deamination is the first step of the metabolic inactivation of [3H]NA induced by tyramine in the cell body of the postganglionic adrenergic neuron while in the nerve endings [3H]NA is preferentially O-methylated.

Animals↗

PubMed2004

The biogenic trace amine tyramine induces a pronounced hydroxyl radical production via a monoamine oxidase dependent mechanism: an in vivo microdialysis study in mouse striatum.

Tyramine is a biogenic trace amine that releases monoamines and is a good substrate for monoamine oxidase (MAO)-A/B. Here we investigated whether tyramine affects hydroxyl radical formation in the intact and lesioned dopaminergic system. Male C57bl/6 mice received systemic and local tyramine administrations. Hydroxyl radical formation and dopamine (DA) overflow were determined in the striatum using in vivo microdialysis in combination with the salicylate hydroxylation assay. Systemic injection of tyramine neither enhanced extracellular dopamine nor induced hydroxyl radical formation. In contrast, when tyramine was incorporated into the dialysate fluid, hydroxyl radical formation and extracellular dopamine levels were significantly enhanced. Systemic pretreatment with the MAO-A/B inhibitor tranylcypromine or with the dopaminergic neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) significantly diminished the tyramine-induced hydroxyl radical formation by 73.1% and 80.6%, respectively. We conclude that the mechanism of tyramine-induced hydroxyl free radical formation involves MAO metabolism and requires an intact dopaminergic system. Pharmacological intervention on the MAO-mediated formation of hydroxyl free radicals seems to be a promising strategy to prevent oxidative damage in the nigrostriatal dopaminergic system.

Animals↗

PubMed2005

Tyramine Functions independently of octopamine in the Caenorhabditis elegans nervous system.

Octopamine biosynthesis requires tyrosine decarboxylase to convert tyrosine into tyramine and tyramine beta-hydroxylase to convert tyramine into octopamine. We identified and characterized a Caenorhabditis elegans tyrosine decarboxylase gene, tdc-1, and a tyramine beta-hydroxylase gene, tbh-1. The TBH-1 protein is expressed in a subset of TDC-1-expressing cells, indicating that C. elegans has tyraminergic cells that are distinct from its octopaminergic cells. tdc-1 mutants have behavioral defects not shared by tbh-1 mutants. We show that tyramine plays a specific role in the inhibition of egg laying, the modulation of reversal behavior, and the suppression of head oscillations in response to anterior touch. We propose a model for the neural circuit that coordinates locomotion and head oscillations in response to anterior touch. Our findings establish tyramine as a neurotransmitter in C. elegans, and we suggest that tyramine is a genuine neurotransmitter in other invertebrates and possibly in vertebrates as well.

Amino Acid Sequence↗

PubMed1983

Blood pressure and plasma norepinephrine concentrations after endogenous norepinephrine release by tyramine.

To determine whether small changes in sympathetic activity would cause detectable changes in plasma norepinephrine (NE) levels, and whether the effects of endogenously released and exogenous NE differ, we injected tyramine infusions and l-norepinephrine (l-NE), into six healthy subjects, and the changes in blood pressure (BP) and plasma NE were related. The mean increase in systolic BP was approximately 17 mm Hg with both infusions; diastolic BP increased with l-NE but did not rise significantly with tyramine. Heart rate fell more with l-NE than with tyramine infusions. The maximum increase in plasma NE levels was more than 500% during l-NE infusions but less than 200% with tyramine. There was no correlation between plasma NE and absolute levels of systolic BP when individual data were plotted for tyramine infusions, whereas mean group changes in systolic BP correlated strongly with mean group plasma NE, both during tyramine and l-NE infusions. The slope of the relationship was much steeper for tyramine than for l-NE. We conclude that the use of plasma NE to measure small differences in sympathetic activity among individuals is limited by interindividual variability, whereas changes in sympathetic activity within groups are more likely to be detected.

Adult↗

PubMed1986

Pressor response of oral tyramine in healthy men given amiflamine and placebo.

During two baseline challenge tests, oral tyramine (50 to 400 mg) was given to 12 healthy men to find each individual's cardiovascular pressor response. All 12 subjects "tolerated" 200 mg oral tyramine, but three of the 12 developed an increment in systolic blood pressure greater than 30 mm Hg when given a dose of 400 mg. Thereafter, amiflamine, 5 mg bid (n = 8), or placebo, 1 capsule twice a day (n = 4), were given in a double-blind fashion for 7 days, and oral tyramine challenge tests (12.5 to 400 mg) were given on days 5 to 7. During dosing with amiflamine or placebo, no subject tolerated 400 mg oral tyramine and no difference between the two regimens was found with regard to tyramine response. Plasma concentrations of amiflamine and two of its metabolites were measured on days 4 to 7. Steady-state concentrations were reached within 4 to 5 days. Plasma concentrations of tyramine after 400 mg tyramine showed a positive correlation with the increase in systolic blood pressure (P less than 0.001).

Administration, Oral↗

PubMed1989

Determination and comparison of the pressor effect of tyramine during long-term moclobemide and tranylcypromine treatment in healthy volunteers.

Monoamine oxidase inhibitors can elicit increases in systolic blood pressure after tyramine ingestion (cheese effect). Moclobemide is a new, reversible, preferential monoamine oxidase A inhibitor with antidepressant properties. Its potentiation of the tyramine pressor effect during 200 mg t.i.d. chronic treatment was compared with tranylcypromine, 10 mg b.i.d., in a double-blind, parallel-group, placebo-controlled study (n = 16). Tyramine was mixed with food and ingested in increasing daily doses, during a normal meal, until a systolic blood pressure increase of at least 30 mm Hg was achieved (tyramine 30). When compared with the usual fasting oral tyramine tests performed in the same subjects, the mean tyramine 30 dose with a meal was 2.8 times higher. The mean tyramine 30 dose with a meal decreased from 1450 mg (range, 800 to 2000 mg) during placebo to 306 mg (range, 150 to 500 mg) during moclobemide (factor, 5.0) and from 1200 mg (range, 1000 to 1600 mg) during placebo to 35 mg (range, 20 to 50 mg) during tranylcypromine (factor, 38.2). The duration of the systolic blood pressure increase was longer with tranylcypromine (126 minutes) than with moclobemide (69 minutes) (p less than 0.01).

Administration, Oral↗

PubMed2000

Tyramine-induced endogenous noradrenaline efflux from in situ cardiac sympathetic nerve ending in cats.

With the use of dialysis technique, the effects of tyramine on in situ cardiac sympathetic nerve endings were examined in anaesthetized cats. Dialysis probes were implanted in the left ventricular myocardium, and the concentration of dialysate noradrenaline (NA) served as an indicator of NA output at the cardiac sympathetic nerve ending. Locally applied tyramine (600 microM) increased dialysate NA levels from 17 +/- 1 (pg mL-1) to 3466 +/- 209 (pg mL-1). Pretreatment with reserpine (vesicle transport NA blocker 1 microM) did not affect tyramine-induced NA efflux. The tyramine-induced NA efflux was augmented by pretreatment with pargyline (1 mM) but suppressed by pargyline (10 mM). Pretreatment with alpha-methyl-tyrosine suppressed NA efflux evoked by tyramine. These pretreatments did not affect the time course of NA efflux but only altered peak height of NA efflux. The efflux of NA evoked by tyramine was not associated with any reduction of dihydroxyphenylglycol (DHPG). In contrast, in the pretreatment with reserpine, the efflux of NA was associated with a reduction of DHPG. This result suggests that NA graduation between axoplasm and stored vesicle contributes to maintaining the axoplasmic NA level during carrier-mediated outward NA transport. The tyramine-induced NA efflux provides a close reflection of the NA content at the nerve ending. With the use of dialysis, this experimental model is suitable for studying the mechanism of sympathomimetic amine-induced neurotransmitter efflux.

Animals↗

PubMed1996

Comparison of the effects of clonidine on tyramine- and methoxamine-evoked mydriasis in man.

1. It has been reported previously that clonidine can potentiate tyramine-evoked mydriasis on the pain-free side of cluster headache patients. We examined whether a single oral dose of clonidine (200 micrograms) can also potentiate tyramine-evoked mydriasis in healthy subjects, using mydriasis to methoxamine, a directly acting sympathomimetic amine, as a control. 2. Eight healthy male volunteers participated in four weekly sessions. In the first two sessions (Experiment 1) the effect of clonidine or placebo on the mydriasis to tyramine hydrochloride eyedrops (75 mM; 2 x 10 microliters), and in the last two sessions (Experiment 2) the effect of clonidine or placebo on the mydriasis to methoxamine hydrochloride eyedrops (20 mM; 2 x 10 microliters) was examined. In both experiments subjects were allocated to drugs and sessions according to a double-blind balanced design. In both experiments, pupil diameter of both the treated and the untreated eyes was recorded in standard ambient light and in the dark, before, and 2 h after clonidine/placebo, via binocular infrared television pupillometry. Salivation (dental roll technique), systolic and diastolic blood pressure (sitting), heart rate, and self-ratings of mood and feelings (visual analogue scales), were also measured before, and 2 h after the ingestion of clonidine or placebo. 3. Both tyramine and methoxamine produced a significant mydriasis, which was more prominent in the light condition (change in resting pupil size; mm +/- s.e.mean: tyramine/light 1.05 +/- 0.28; tyramine/dark: 0.73 +/- 0.15; methoxamine/light: 1.65 +/- 0.28; methoxamine/dark: 0.85 +/- 0.15). Clonidine produced a significant miosis in the untreated eye which was more prominent in the light condition (change in resting pupil size; mm +/- s.e.mean: Experiment 1, light: -1.34 +/- 0.19; Experiment 1, dark: -0.46 +/- 0.1; Experiment 2, light -0.97 +/- 0.18; Experiment 2, dark: -0.29 +/- 0.17). Clonidine had no significant effect on either tyramine- or methoxamine-evoked mydriasis. 4. In agreement with previous reports, clonidine significantly reduced salivation (g, mean +/- s.e.mean; Experiment 1: -0.84 +/- 0.22; Experiment 2: -0.55 +/- 0.11), systolic blood pressure (mm Hg; Experiment 1: -17.5 +/- 3.76; Experiment 2: -23.38 +/- 4.67), diastolic blood pressure (mm Hg; Experiment 2: -12.38 +/- 2.05), alertness (mm; Experiment 2: -24.19 +/- 5.40), and anxiety (mm; Experiment 1: -13.82 +/- 4.60), indicating the presence of pharmacodynamically effective tissue levels of the drug. 5. These results show that a single oral dose (200 micrograms) of clonidine causes significant miosis in human subjects, and fails to potentiate tyramine-evoked mydriasis. This indicates that the pupil on the asymptomatic side of cluster headache patients is affected differently from the pupils of healthy volunteers by tyramine and/or clonidine.

Adolescent↗

PubMed2000

Isolation, properties and behaviour of tyramine-producing lactic acid bacteria from wine.

Wines containing high levels of biogenic amines were investigated for the presence of tyramine-producing strains. Two different Lactobacillus brevis (IOEB 9809 and IOEB 9901) able to produce the amine were isolated. None of the isolated strains identified as Oenococcus oeni formed tyramine. In addition, other Lact. brevis and Lact. hilgardii strains from our collection (IOEB) and the American Type Culture Collection (ATCC) were strong tyramine producers. Lactobacillus brevis IOEB 9809 and Lact. hilgardii IOEB 9649 were found to produce tyramine and phenylethylamine simultaneously. The conditions that can influence tyramine formation in wine were evaluated for three strains of Lact. brevis (IOEB 9809 and IOEB 9901) and Lact. hilgardii (IOEB 9649). Tyrosine was the major factor affecting tyramine formation and was enhanced by the presence of sugars, mainly glucose. Tyrosine decarboxylase (TDC) activity greatly depended on the presence of the precursor, which suggested that tyrosine induced the TDC system. These results indicate that Lactobacillus could be the lactic acid bacteria responsible for tyramine production in wine.

Lactobacillus↗

PubMed1994

Competitive binding of low molecular mass heparin-tyramine fluorescein-5-isothiocyanate and unlabeled glycosaminoglycans to leukocytes.

Antithrombotic, antiarteriosclerotic, and anti-inflammatory actions of heparins may be mediated by binding of heparin to leukocytes. To get the first information on this hypothesis, fluorescein-labeled LMMH-tyramine has been used (LMMH-tyramine-FITC) to analyze the binding of GAGs to lymphocytes, monocytes, or granulocytes. The fluorescence intensity on leukocytes was quantified by flow cytometry analysis. LMMH-tyramine-FITC bound dose dependently to lymphocytes, monocytes, and granulocytes. PE-labeled CD 11c antibodies identified the specificity of the binding of LMMH-tyramine-FITC to granulocytes. UFH and LMMH displaced LMMH-tyramine-FITC dose dependently from leukocytes. Equimolar ratios of LMMH and LMMH-tyramine-FITC revealed a 50% displacement of the labeled compound, indicating the specific binding by the polysaccharide chain. The synthetic pentasaccharide was 10-fold and dermatan sulfate 100-fold less effective than UFH in displacing LMMH-tyramine-FITC from leukocytes. The data indicate that negatively charged GAGs bind to the surface of lymphocytes, monocytes, and granulocytes. By decreasing the number of negatively charged groups of GAGs, the binding to the surface of leukocytes is decreased. The data obtained with the synthetic pentasaccharide indicate a binding of GAGs to the surface of leukocytes, independently of AT III. The cellular binding of heparins may significantly contribute to its antithrombotic and other biologic activities.

Antigen-Antibody Reactions↗

PubMed2004

Effect of oral linezolid on the pressor response to intravenous tyramine.

AIMS: To investigate the effect of monoamine oxidase A inhibition from a single oral dose of linezolid on the pressor response to intravenous (i.v.) tyramine, using positive and negative controls to validate the methodology. METHODS: This placebo-controlled, three-period crossover study was conducted in 12 healthy male volunteers. Each volunteer received either one oral dose of moclobemide (300 mg), linezolid (600 mg), or placebo tablet followed by an i.v. tyramine pressor test until an increase in systolic blood pressure of at least 30 mmHg above baseline occurred. Each study day was separated by a 7-day washout period. The dose of tyramine required to raise the blood pressure by 30 mmHg (TYR30) was calculated for each oral treatment by linear interpolation between log-transformed doses of i.v. tyramine. The influence of body mass index (BMI) on TYR30 was also investigated. RESULTS: The tyramine sensitivity factor (ratio of the geometric least square mean TYR30 for placebo and active oral treatment) was 1.8 [90% confidence interval (CI) 1.6, 2.0, P < 0.0001] for linezolid and 2.1 (90% CI 1.8, 2.4, P < 0.0001) for the positive control moclobemide. BMI had a statistically significant effect on TYR30. CONCLUSIONS: There was a significant difference in the pressor response to i.v. tyramine between linezolid and placebo. Moclobemide (positive control) and linezolid have a similar pressor response to i.v. tyramine. The statistically significant effect of BMI on TYR30 underlines the advantage of within-individual comparisons of treatments in order to reduce variability and provide more accurate treatment estimates.

Acetamides↗

PubMed1990

In vivo mechanisms underlying dopamine release from rat nigrostriatal terminals: II. Studies using potassium and tyramine.

The brain microdialysis technique has been used to examine the in vivo effects of potassium and tyramine on dopamine (DA) release and metabolism in the striatum of halothane-anaesthetised rats. Increasing the concentration of potassium perfusing the dialysis probe (30-120 mM) induced a dose-related efflux of DA. A dose-related release of DA was also observed following addition of tyramine (1-100 microM) to the perfusing buffer. High concentrations of potassium were found to reduce the dialysate content of the DA metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid and the serotonin metabolite 5-hydroxyindoleacetic acid. No such effect was observed even when using the highest concentration of tyramine tested. Potassium-evoked DA release was facilitated by pretreatment with the DA uptake inhibitor nomifensine, was inhibited by depletion of extracellular calcium, and was not significantly affected by tetrodotoxin (TTX). The effect of tyramine on DA efflux was inhibited by nomifensine and was insensitive to both TTX and calcium depletion. These data suggest that potassium and tyramine induce release of DA via different mechanisms. Potassium-induced DA release involves a carrier-independent process and may utilise an exocytotic release mechanism. On the other hand, tyramine-induced DA release would appear to involve a carrier-dependent process. Depletion of vesicular stores of DA by pretreatment with reserpine did not significantly affect potassium-induced DA release, whereas a marked inhibition of the effects of tyramine was noted. However, in reserpinised animals the potassium-induced release of DA was inhibited by nomifensine, a result suggesting that a carrier-dependent release mechanism operates in the absence of vesicular DA.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗