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PubMed2001

[New development of hair examination! The searching of hair for the terminal residual substance of pleasant sensation].

Formerly, hair had been analyzed mainly in the field of individual identification. Otherwise, it is known that many substances are accumulated in hair such as metals like arsenic, mercury, alkaloids like caffeine, theophylline, drugs like opiate, stimulants, other drugs and poisons. So, by qualitative and quantitative analysis of such deposits in hair. It is possible to presume one's life manner during recent several months. This is the new development of hair analysis and it is expected that it may be wide of application. The main theme of this paper is hedonics. Nobody dislike hedonic sensation. So, it can be said everybody being living always coveting hedonic sensation. There are many hedonic sensers all over the body, and hedonic sensation transmitted by A10 nerve, so A10 nerve is called the hedonic nerve. Neurotransmitter of this A10 nerve is Dopamine. Dopamine is the endogenous hedonic material. Exogeneous hedonic one is stimulant like Methamphetamine. In this paper, relation between Dopamine, Methamphetamine and Tyramine, thought to be the terminal product from two formers is examined in the aspect of hair analysis. Catecholamines including Dopamine are made of Tyrosine. They have a Benzene-ring. Compounds with a Benzene-ring made of Tyrosine are relatively rare, but all of them have very strong action. Tyramine is made of Tyrosine, too. So the structure of Tyramine is essentially resemble to Dopamine, and the skeletal structure of Methamphetamine is identical to Dopamine, so the action is identical, too. Normally, excessive release of Dopamine in brain is controlled by the negative feedback of GABA system. But extrinsic stimulus as Methamphetamine put balance of the homeostasis between Dopamine system and GABA system in to disorder, and long term administration of Methamphetamine makes long remaining degeneration of synapse of Dopamine nerve. So, abnormal state of excess releasing of Dopamine happens easily. And the morbid state named stimulant psychosis occur. The volume of Tyramine in hair changes correlatively with the volume of released Dopamine in brain. Therefore it is suggested that quantitative analysis of Tyramine in hair enable to estimate the changes of Dopamine released in brain.

Amphetamine↗
PubMed1990

[Modulation of norepinephrine release in sympathetic nerve endings in renal hypertensive dogs].

Experimental renal hypertensive and normal dogs with femoral arteries constantly perfused were studied. Cocaine was used to block the presynaptic norepinephrine (NE) reuptake and tyramine to initiate the release of NE in sympathetic nerve endings. NE spillover and infusion pressure were measured under basic conditions and during intraarterial infusion of cocaine, tyramine and in combination with alpha 1 and alpha 2 adrenoceptor antagonists. The extent of NE spillover increase induced by infusion of tyramine, the increased infusion pressure by cocaine and tyramine, and the reduced infusion pressure by prazosin were all greater in hypertensive dogs than those in normal dogs, but adrenoceptor antagonist idazoxan further increased tyramine-induced NE spillover in normal dogs only. It was suggested that reduced-regulation of presynaptic alpha 2 adrenoceptors to NE release and increased responsiveness of postsynaptic alpha 1 adrenoceptors to NE were present in hypertensive dogs.

Adrenergic alpha-Antagonists↗
PubMed1991

Lysosomal and endosomal heterogeneity in the liver: a comparison of the intracellular pathways of endocytosis in rat liver cells.

Air-filled albumin microspheres, asialoorosomucoid and formaldehyde-treated serum albumin are selectively taken up by endocytosis in rat liver Kupffer cells, parenchymal cells and endothelial cells, respectively. Intracellular transport and degradation of endocytosed material were studied by subcellular fractionation in sucrose and Nycodenz gradients after intravenous injection of the ligand. By using ligands labeled with 125I-tyramine-cellobiose, the subcellular distribution of labeled degradation products can be studied because they are trapped at the site of formation. The results show that the kinetics of intracellular transport are different in hepatic parenchymal, endothelial and Kupffer cells. In endothelial cells, the ligand is associated with two types of endosomes during the first minutes after internalization and then is transferred rapidly to the lysosomes. In parenchymal cells, 125I-tyramine-cellobiose-asialoorosomucoid was located in a relatively slowly sedimenting vesicle during the first minute after internalization and subsequently in denser endosomes. Degradation of 125I-tyramine-cellobiose-asialoorosomucoid in parenchymal cells started later than that of 125I-tyramine-cellobiose-formaldehyde-treated serum albumin in endothelial cells. Furthermore, the ligand seemed to be transferred relatively slowly from endosomes to lysosomes, and most of the undegraded ligand was in the endosomes. The rate-limiting step of proteolysis in parenchymal cells is probably the transport from endosomes to lysosomes. In Kupffer cells, most 125I-tyramine-cellobiose-microspheres are found as undegraded material in very dense endosomes up to 3 hr after injection. After 20 hr, most of the ligand is degraded in lysosomes distributed at a lower density than the endosomes in Nycodenz and sucrose gradients.

Albumins↗
PubMed1985

Differences between exogenous and endogenous noradrenaline in the effects on vascular post-synaptic alpha 1- and alpha 2-adrenoceptors in man.

Effects of exogenous and endogenous noradrenaline, released by tyramine and lower body negative pressure (LBNP), on vascular post-synaptic alpha 1- and alpha 2-adrenoceptors have been compared in healthy volunteers. Intra-arterial (i.a.) infusions of noradrenaline and tyramine into the forearm were given in the presence of saline, of yohimbine and of doxazosin, and changes in forearm blood flow (FBF) were measured. Lower body negative pressure of -40 mmHg was applied without and with a continuous i.a. infusion of yohimbine and of doxazosin, and changes in FBF in both forearms were compared. Forearm blood flow was measured by venous occlusion plethysmography. Noradrenaline and tyramine reduced FBF dose-dependently and to the same extent. Both these vasoconstrictions were significantly reduced by yohimbine (P < 0.001 for both) as well as by doxazosin (P < 0.05 for noradrenaline and P < 0.001 for tyramine). The tyramine-induced vasoconstriction was more effectively reduced by doxazosin, whereas yohimbine reduced the noradrenaline-induced vasoconstriction more effectively. Lower body negative pressure reduced FBF in both forearms to the same extent. Doxazosin effectively inhibited the LBNP induced decrease in FBF (P < 0.05) whereas yohimbine had no effect (P > 0.05). These results are in accordance with a predominant intrasynaptic location of post-synaptic alpha 1-adrenoceptors and a predominant extrasynaptic location of post-synaptic alpha 2-adrenoceptors in human blood vessels.

Adult↗
PubMed1986

Evidence for an ascorbate shuttle for the transfer of reducing equivalents across chromaffin granule membranes.

Adrenal chromaffin granules must shuttle reducing equivalents from the cytosol inward to reduce ascorbic acid oxidized during norepinephrine biosynthesis by intragranular dopamine-beta-hydroxylase. A transmembrane electron shuttle between the external (cytosolic) and intragranular ascorbate pools was demonstrated in vitro in intact bovine chromaffin granules undergoing tyramine- or dopamine-stimulated dopamine-beta-hydroxylase turnover. Incubation of intact chromaffin granules with tyramine results in a time-dependent decrease in reduced intragranular ascorbate and production of octopamine. The rate of ascorbate oxidation is a function of the extragranular concentrations of tyramine over the range 50 microM to 2 mM and is 95% inhibited by addition of the dopamine-beta-hydroxylase inhibitor disulfiram. The stoichiometry of octopamine synthesized/ascorbate oxidized closely approximates unity. The presence of extragranular dopamine also induces oxidation of intragranular ascorbate which is inhibited by blocking dopamine transport with reserpine. On the other hand, incubation with octopamine, which is also transported by the granules, causes no net decrease in reduced intragranular ascorbate. The presence of 400 microM extragranular ascorbate abolishes the observed tyramine-induced intragranular ascorbate oxidation. The addition of ascorbate extragranularly 30 min after addition of tyramine reverses the oxidation of intragranular ascorbate. The measurement of [14C]ascorbate distribution ratios in granule pellets and supernatants indicates that there is no transmembrane transport of ascorbate. Extravesicular NADH had no significant effect on matrix ascorbate levels during beta-hydroxylation. These data provide new in vitro evidence that chromaffin granules shuttle reducing equivalents inwardly from an extra- to an intravesicular ascorbate pool and that cytosolic ascorbate is the source of the intragranular reducing equivalents required during norepinephrine biosynthesis.

Animals↗
PubMedDate not supplied

[Involvement of monoamine oxidases in formation of 4-hydroxyphenylethanol, major component of tribulin A].

Pathways of 4-hydroxyphenylethanol formation were studied in the bovine brain. Incubation of brain homogenates with tyramine or tyrosine increased 4-hydroxyphenylethanol content only in the presence of NADH. Tyramine produced more pronounced augmentation of 4-hydroxyphenylethanol content than tyrosine. Tyrosine preparations were not contamined with tyramine. This suggests that 4-hydroxyphenylethanol may be formed from tyramine and tyrosine in NADH-dependent process. Preincubation of homogenates with 0.1 mM pargyline completely inhibited monoamine oxidases A and B and prevented NADH-dependent formation of 4-hydroxyphenylethanol from tyramine. The latter suggests that MAO is involved in formation of 4-hydroxyphenylethanol.

Adrenergic alpha-Antagonists↗
PubMed1998

Cocaine acts as an apparent competitive inhibitor at the outward-facing conformation of the human norepinephrine transporter: kinetic analysis of inward and outward transport.

The inhibition by cocaine of inward and outward transport of dopamine (DA) at the cloned human norepinephrine transporter (hNET) and the relationship of the inhibitory patterns of cocaine to the conformational requirements of the transporter were investigated. This was done using rotating disk electrode voltammetry in transfected cells. The uphill uptake of external DA, the lack of inhibition by internal substrates on DA uptake, and the accelerated exchange of internal DA by external m-tyramine support a carrier model in which the hNET alternates between outward-facing and inward-facing conformations. Cocaine exhibited competitive inhibition of DA uptake, which was insensitive to intracellular substrates. In contrast, the inhibition by cocaine of the m-tyramine-induced DA efflux appeared noncompetitive relative to intracellular DA, but competitive relative to extracellular m-tyramine. Simultaneous measurement of m-tyramine uptake and accompanying DA efflux at various concentrations of intracellular DA showed that cocaine did not alter the ratio of DA efflux to m-tyramine uptake. Moreover, cocaine displayed similar potency for inhibiting DA uptake and efflux. Additionally, the inhibition profile of cocaine was unrelated to the addition time of cocaine, simultaneously with or earlier than a substrate. All of the findings are consonant with a competitive interaction between cocaine and substrates at the outward-facing conformation of the hNET. This action directly prevents the inward transport of external substrates, thereby inhibiting the outward transport of internal substrates by reducing the availability of the inward-facing conformation. Consequently, the experimental inhibition pattern of cocaine depends on the conformation of the hNET to which the transported substrate is exposed.

Animals↗
PubMed1990

Inhibition of dopamine beta-hydroxylase by bidentate chelating agents.

1-2H-Phthalazine hydrazone (hydralazine; HYD), 2-1H-pyridinone hydrazone (2-hydrazinopyridine; HP), 2-quinoline-carboxylic acid (QCA), 1-isoquinolinecarboxylic acid (IQCA), 2,2'-bi-1H-imidazole (2,2'-biimidazole; BI), and 1H-imidazole-4-acetic acid (imidazole-4-acetic acid; IAA) directly and reversibly inhibit homogeneous soluble bovine dopamine beta-hydroxylase (3,4-dihydroxyphenethylamine, ascorbate:oxygen oxidoreductase (beta-hydroxylating), EC 1.14.17.1). HYD, QCA and IAA show competitive allosteric inhibition of dopamine beta-hydroxylase with respect to ascorbate (Kis = 5.7(+/- 0.9) microM, 0.14(+/- 0.03) mM, 0.80(+/- 0.20) mM; nH = 1.4(+/- 0.1), 1.8(+/- 0.4), 2.8(+/- 0.6), respectively). HYD and IAA show slope and intercept mixed-type allosteric inhibition of dopamine beta-hydroxylase with respect to tyramine. QCA shows allosteric uncompetitive inhibition of dopamine beta-hydroxylase with respect to tyramine. HP, BI and IQCA all show linear competitive inhibition (Kis = 1.9(+/- 0.3) microM, 21(+/- 6) microM, and 0.9(+/- 0.3) microM, respectively) with respect to ascorbate. HP and BI show linear mixed-type while IQCA shows linear uncompetitive inhibition of dopamine beta-hydroxylase with respect to tyramine. In the presence of HP, HYD or IAA intersecting double-reciprocal plots of the initial velocity as a function of tyramine concentration at differing fixed levels of ascorbate are observed. These findings are consistent with a uni-uni-ping-pong-ter-bi kinetic mechanism for dopamine beta-hydroxylase that involves a ternary enzyme-ascorbate-tyramine-oxygen complex. The results for HYD, QCA and IAA are the first examples of allosteric inhibitor interactions with dopamine beta-hydroxylase.

Animals↗
PubMedDate not supplied

[In vitro and in vivo production of amines by a Lactobacillus strain isolated from a cock crop].

The chicken digestive tract is mainly colonized by bacteria belonging to the Lactobacillus genus. One of these strains (LEM-207) isolated from the crop of a cock and closely resembling L. acidophilus, was able to develop on a carbohydrate-free medium. Production of carbon dioxide and synthesis of tyramine, putrescine and cadaverine were observed in the cultures. Once implanted in the crops of germ-free chickens, strain LEM-207 led to the formation of amines. In germ-free (axenic) animals, only endogenous tyramine was detected, whereas in monoassociated chickens, we found a production of tyramine, cadaverine and putrescine. The concentrations of cadaverine and putrescine decreased with increasing acidification of the contents, whereas the level of tyramine increased (7-fold higher level than in germ-free chicken). Amine production was not detected in the caeca. The toxicological aspects of tyramine production in terms of the animal are discussed.

Amines↗
PubMed1997

Selective inhibitors of monoamine oxidase. 4. SAR of tricyclic N-methylcarboxamides and congeners binding at the tricyclics' hydrophilic binding site.

Linear [6.6.6] tricyclic moieties whose center ring is made of two atoms of differing size (here primarily thioxanth-9-ones and phenoxathiins) monosubstituted meta to the sulfur by C(O)NHMe include potent and selective inhibitors of monoamine oxidase A. Similarities with effects on SAR of acylamide and of diazapentacyclic substitution on such rings, including positional variables, the requirement for monomethylation (primary and dialkylated amides are inactive and higher monoalkylated amides show little or no potency), and that sulfur is optimally in sulfone form, suggest that binding to the enzyme occurs similarly in each series. No significantly greater rise in blood pressure was found in rats given sufficient 8 to inhibit most brain and liver MAO A and then followed by oral tyramine than was found on administration of tyramine to controls. This is in contrast to a large blood pressure rise in rats pretreated with phenelzine followed by tyramine, and in accord with the belief that an inhibitor selective for MAO A which is reversibly bound to the enzyme and therefore displaced by any ingested tyramine will not lead to the "cheese effect" (hypertension during treatment with MAO inhibitors usually caused by ingestion of foods containing tyramine).

Animals↗
PubMed1990

Reabsorption and intracellular transport of cytochrome c and lysozyme in rat kidney.

Renal uptake and degradation of cytochrome c and lysozyme were investigated, using preparations that were labelled by means of covalent coupling of either protein to iodinated tyramine-cellobiose. Following proteolytic digestion, the label remains 'trapped' within intracellular organelles. Within 15 min after intravenous injection, 43% of the [125I]tyramine-cellobiose-cytochrome c and 29% of the [131I]tyramine-cellobiose-lysozyme were recovered in the kidneys. Isopycnic sucrose-gradient fractionation indicates that the two proteins initially exhibit closely similar intracellular distributions, being associated with vesicles of an equilibrium density slightly lower than that of plasma membranes. However, within 5 min after injection, the two proteins exhibit distinctly different distribution profiles. The [125I]tyramine-cellobiose-cytochrome c is localized predominantly in the lysosomal fraction of the gradient. The [131I]tyramine-cellobiose-lysozyme is also translocated to the lysosomal fraction, but at a much lower rate. For both proteins, the rates of intracellular degradation correlate with their rates of translocation. The observed difference in their kinetics of intracellular movement suggests that the two proteins are translocated at different rates into transport vesicles.

Absorption↗
PubMed2002

Is sympathetic neural vasoconstriction blunted in the vascular bed of exercising human muscle?

Sympathetic vasoconstriction of muscle vascular beds is important in the regulation of systemic blood pressure. However, vasoconstriction during exercise can also compromise blood flow support of muscle metabolism. This study tested the hypothesis that local factors in exercising muscle blunt vessel responsiveness to sympathetic vasoconstriction. We performed selective infusions of three doses of tyramine into the brachial artery (n = 8) to evoke endogenous release of noradrenaline (norepinephrine) at rest and during moderate and heavy rhythmic handgrip exercise. In separate experiments, tyramine was administered during two doses of adenosine infusion (n = 7) and two doses of sodium nitroprusside (SNP) infusion (n = 8). Vasoconstrictor effectiveness across conditions was assessed as the percentage reduction in forearm vascular conductance (FVC), calculated from invasive blood pressure and non-invasive Doppler ultrasound blood flow measurements at the brachial artery. Tyramine evoked a similar dose-dependent vasoconstriction at rest in all three groups, with the highest dose resulting in a 42-46 % reduction in FVC. This vasoconstriction was blunted with increasing exercise intensity (e.g. tyramine high dose percentage reduction in FVC; rest -43.4 +/- 3.7 %, moderate exercise -27.5 +/- 2.3 %, heavy exercise -16.7 +/- 3.6 %; P < 0.05). In contrast, tyramine infusion resulted in a greater percentage reduction in FVC during both doses of adenosine vs. rest (P < 0.05). Finally, percentage change in FVC was greater during low dose SNP infusion vs. rest (P < 0.05), but not different from rest at the high dose of SNP infusion (P = 0.507). A blunted percentage reduction in FVC during endogenous noradrenaline release in exercise but not vasodilator infusion indicates that sympathetic vasoconstriction is blunted in exercising muscle. This blunting appears to be exercise intensity-dependent.

Adenosine↗
PubMed2000

Reduction of biogenic amine formation using a negative amino acid-decarboxylase starter culture for fermentation of Fuet sausages.

The ability of Lactobacillus sakei CTC494, a negative amino acid-decarboxylase starter culture, to reduce biogenic amine accumulation during sausage fermentation and storage at 4 and 19 degrees C was studied. The effect on the amine formation of the tyramine producer Lactobacillus curvatus CTC371, as a positive strain, was also examined in comparison to a spontaneous fermentation process without starter culture (control batch). The polyamines spermine, spermidine, and diaminopropane were not influenced by the ripening, and their levels slightly decreased in all the batches throughout the storage. Tyramine, cadaverine, and putrescine were the main amines formed during the ripening. The addition of starter culture resulted in a decrease on the biogenic amine formation, depending on the strain inoculated. A great reduction in tyramine content was achieved when L. sakei CTC494 was inoculated, whereas L. curvatus CTC371 only attenuated tyramine accumulation compared with the control batch. Both starters were able to significantly limit the production of putrescine and cadaverine, and they inhibited tryptamine and phenylethylamine formation by the wild microbial flora. Tyramine levels of the control sausages rose during the storage at both temperatures, whereas those of cadaverine only increased at 19 degrees C. On the contrary, sausages manufactured through the starter controlled fermentation did not show changes of amine contents during the storage. The addition of a proper selected starter culture is advisable to produce safer sausages with low contents of biogenic amines.

Animals↗
PubMed1986

[Organ distribution of ruthenocenyl biogenic amine derivatives--radiodiagnostic agents for the adrenals and ovaries?].

The organ distribution of 103Ru labelled ruthenocenyl derivatives of tyramine, histamine, benzylamine, phenylethylamine and homoveratrylamine were measured in rats. The derivatives of tyramine, histamine and benzylamine showed a high affinity for the adrenal and ovar. Adrenal/muscle ratios up to 2000:1 were gained but only if the dose was administered i.v. and was below 0.1 mumol/kg. The ruthenocenyl derivatives of tyramine labelled with 103Ru in the ruthenocene moiety or with 14C in the tyramine moiety showed a parallel distribution pattern but completely different from the distribution of 103RuCl3. This indicates that the tyramine derivatives are not destroyed in the body yielding Ru-ions. The advantages of the ruthenocenyl derivatives in comparison with the known amphetamine derivatives labelled with radioactive iodine are discussed.

Adrenal Glands↗
PubMed1984

Alternate substrates of dopamine beta-hydroxylase. I. Kinetic investigations of benzyl cyanides as substrates and inhibitors.

A series of benzyl cyanide analogs have been studied as substrates and inhibitors of dopamine beta-hydroxylase to extend our initial report (Baldoni, J. M., and Villafranca, J. J. (1980) J. Biol. Chem. 255, 8987-8990) which showed that p-hydroxybenzyl cyanide was a suicide substrate of dopamine beta-hydroxylase. Thus, the appVmax values for benzyl cyanide analogs decrease in the order p-OH greater than m-OH greater than H much greater than p-OCH3,m-OCH3; the m-OH, m-OCH3 and p-OCH3 analogs are competitive inhibitors versus tyramine in initial velocity studies. The Vmax values for tyramine and p-hydroxybenzyl cyanide are nearly identical at saturating O2 and ascorbate (pH 5.0, 37 degrees C) but the Km for O2 is 0.14 and 2.8 mM, respectively, with tyramine and p-hydroxybenzyl cyanide. Studies of the pH dependence of log V/K for tyramine show two pKa values of 5.2 and 5.8 while for m-hydroxybenzyl cyanide the values are 5.3 and 5.9. The log Vmax profile shows one pKa of 5.9 with tyramine as substrate. Thus, nearly identical enzymic groups are involved in binding and/or catalysis with these two substrates. All the benzyl cyanide analogs are suicide inactivators of dopamine beta-hydroxylase. With m-hydroxybenzyl cyanide, the partition between catalysis and inactivation (kcat/kinact) changed from approximately 600 to approximately 17 as the pH varied from 5.0 to 6.7. The log kinact versus pH profile shows one pKa value of 6.0, suggesting that an enzymic group must be deprotonated for maximal inactivation. Copper was essential for the suicide inactivation of dopamine beta-hydroxylase by benzyl cyanides and kinetic studies of partially inhibited dopamine beta-hydroxylase (approximately 50%) showed that inactive enzyme molecules were completely inactive. The following papers in this series discuss the partial reactivation of suicide-inhibited dopamine beta-hydroxylase and the stoichiometry of inactivation by benzyl cyanide analogs.

Adrenal Medulla↗
PubMed1988

The handling of five amines by the extraneuronal deaminating system of the rat heart.

The handling of five amines by the extraneuronal deaminating system was studied in perfused hearts of rats (pretreated with reserpine; COMT and neuronal uptake inhibited). Hearts were perfused with 50 nmol/l 3H-noradrenaline for 30 min, in the presence of increasing concentrations of unlabelled (-)-adrenaline, (-)-noradrenaline, dopamine, tyramine and 5-HT. IC50's were determined as those concentrations of unlabelled amines which halved the steady-state rate of deamination of 3H-noradrenaline. After correction for changes in the tissue/medium ratio for 3H-noradrenaline, "half-saturating outside concentrations" were obtained. They increased in the order (-)-adrenaline (15 mumol/l) - tyramine - dopamine - noradrenaline - 5-HT (53 mumol/l). The Vmax for extraneuronal deamination was determined for 3H-(-)-adrenaline, 3H-(-)-noradrenaline and 3H-dopamine, as well as (by HPLC and electrochemical detection) for tyramine and 5-HT. It was low for (-)-adrenaline, intermediate for (-)-noradrenaline, dopamine and 5-HT, high for tyramine. For the three catecholamines the half-saturating outside concentrations of the extraneuronal deaminating system clearly exceeded those for the extraneuronal O-methylating system of the same organ (see Grohmann and Trendelenburg 1985), although the two enzymes appear to co-exist in the same cells, so that the same transport system is involved.

Animals↗
PubMed1977

Pargyline-induced increases in sensitivity to the effects of drugs on operant behavior in pigeons.

Pigeons responded under a multiple fixed-interval 5-min, 30-response fixed-ratio schedule of food reinforcement. Acute pargyline doses between 10.0 and 50.0 mg/kg (i.m.); given immediately prior to the session, decreased responding. Daily administration of 50 mg/kg pargyline (24 mg/kg, every 12 hr) initially decreased responding. Tolerance developed so that after 4 days of daily pargyline, responding had returned to control values. Chronic pargyline resulted in an enhanced sensitivity to the effects of d-amphetamine, ephedrine, tyramine, and morphine on schedule-controlled responding. Both d-amphetamine and pentobarbital increased fixed-interval responding at relatively low doses, while higher doses decreased responding. Daily pargyline resulted in an increased sensitivity to both the increases and decreases in response rates produced by d-amphetamine. In contrast, sensitivity to pentobarbital was not changed after daily pargyline, Ephedrine, tyramine, and morphine only decreased fixed-interval responding. Chronic pargyline resulted in an increased sensitivity to the response-rate decreasing effects of ephedrine, tyramine, and morphine. In addition to the increased sensitivity of fixed-interval responding to the effects of tyramine, the dose-effect curve for fixed-ratio responding was also a shifted to the left. Daily pargyline did not result in changes in sensitivity of fixed-ratio responding to the effects of the other drugs tested.

Animals↗
PubMed1984

Selective inhibition by amiflamine of monoamine oxidase type A in rat brain, liver and duodenum.

Amiflamine (FLA 336(+)), N-desmethylamiflamine (FLA 788(+)) and N,N-didesmethylamiflamine (FLA 668(+)) were examined for their monoamine oxidase (MAO) inhibitory effects in rat brain, liver and duodenum and were compared with the irreversible inhibitors clorgyline and (-)-deprenyl. The potency of each FLA compound was the same in each tissue both in vitro and after oral administration with either serotonin or tyramine as substrate. The in vitro effect of FLA 788(+) was 2-6 times stronger than that of amiflamine although the compounds were equipotent after oral administration. FLA 668(+) was 2-3 times less potent than amiflamine in vitro and had very poor activity after oral administration. The deamination of phenethylamine was weakly affected by the three FLA compounds. Clorgyline inhibited strongly the deamination of serotonin and tyramine in the duodenum after oral administration, being 1,000 times more potent than in the brain and the liver. Similar results were obtained for (-)-deprenyl which, however, was more potent in inhibiting the deamination of phenethylamine than that of serotonin and tyramine. Amiflamine was a reversible MAO inhibitor with no MAO inhibitory capacity 24 h after a single oral dose. On the other hand the irreversible inhibitor clorgyline had a maximal effect on brain MAO 48 h after a single dose while the inhibitory effect in the duodenum had almost disappeared. The influence of amiflamine on the excretion of acid and basic metabolites of orally administered 14C-tyramine (58 mumol/kg) in rat was examined.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗