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  • 1
    Electronic Resource
    Electronic Resource
    Phenylethylamine-induced stereotypies in the rat: a behavioral test system for assessment of MAO-B inhibitors (1984)
    Springer
    Psychopharmacology 84 (1984), S. 22-27 
    Details
    ISSN: 1432-2072
    Keywords: Phenylethylamine levels ; MAO-B inhibitor ; Stereotyped behavior
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Stereotyped sniffing behavior together with forepaw padding — defined as the β-phenylethylamine (PEA) syndrome — is induced by MAO-B inhibitors in rats injected with 30 mg/kg IP PEA. The comparison of the abilities of the MAO-B inhibitors to induce the syndrome and to inhibit MAO-B in rat brain homogenates indicated that at least 75% of MAO-B activity in rat brain had to be inhibited to induce the PEA syndrome. A good correlation was found between the abilities of MAO-B inhibitors to induce the behavioral syndrome and to increase levels of PEA in rat brain. Specific MAO-A inhibitors potentiated the behavioral effect of the MAO-B inhibitor deprenyl, while they did not induce the syndrome themselves or only at very high doses. Inhibitors of the reuptake of 5-HT or noradrenaline were inactive under the described experimental conditions. This behavioral test system seems to be useful in vivo screening test in rats for detecting compounds with strong MAO-B inhibiting activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00432018
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  • 2
    Electronic Resource
    Electronic Resource
    The effects of 5-HT uptake- and MAO-inhibitors on l-5-HTP-induced excitation in rats (1980)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 311 (1980), S. 185-192 
    Details
    ISSN: 1432-1912
    Keywords: Serotonin behaviour ; l-5-HTP syndrome ; 5-HT uptake inhibitors ; MAO inhibitors ; 5-HT
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The behavioural syndrome caused by l-5-HTP in rats was used for the study of effects of selective 5-HT uptake inhibitors and inhibitors of MAO on central 5-HT receptors. A good correlation was found between the relative potencies of drugs in inhibiting the 5-HT uptake in the rat brain and in intensifying l-5-HTP-induced behavioural stimulation. The potentiation of the l-5-HTP syndrome by the MAO inhibitors correlated with the inhibition of the A- but not of the B-form of the brain monoamine oxidase. In rats treated with the maximally inhibiting dose of a 5-HT uptake inhibitor, MAO inhibitors were still able to increase the intensity of the l-5-HTP syndrome, while the combination of maximal doses of two 5-HT uptake inhibitors did not produce a more intense syndrome than that produced by one 5-HT uptake inhibitor alone. The l-5-HTP-induced behavioural syndrome in rats seems to afford an experimental model allowing the quantification and characterization of the interaction of drugs with serotonin metabolism in the brain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00510258
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  • 3
    Electronic Resource
    Electronic Resource
    3-methoxytyramine: Its suitability as an indicator of synaptic dopamine release (1981)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 315 (1981), S. 219-225 
    Details
    ISSN: 1432-1912
    Keywords: 3-Methoxytyramine ; Haloperidol ; Dopamine release ; Dopamine agonists ; Gas chromatography ; Mass Spectrometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The value of 3-methoxytyramine (3-MT) as an indicator of impulse-related dopamine (DA) release has been assessed in rat corpus striatum. Moreover, the turnover of 3-MT was estimated by measuring its disappearance rate after COMT inhibition. Quantitation of 3-MT and DA was performed by gas chromatography/mass spectrometry (selected ion monitoring). Haloperidol in doses between 0.05 and 3 mg/kg p.o. did not increase endogenous 3-MT levels at any time up to 24 h after its administration, whereas it dose-dependently increased homovanillic acid and 3,4-dihydroxyphenylacetic acid. However, in doses above 0.1 mg/kg p.o., it enhanced the accumulation of 3-MT in clorgyline-pretreated animals. Conversely, baclofen in doses of 2 mg/kg i.p. and above decreased endogeneous 3-MT levels, but reduced the accumulation of this amine only poorly at 20 mg/kg i.p. in clorgyline-pretreated rats. A number of dopamine agonists, apomorphine (0.5 mg/kg i.v.), dipropyl-ADTN (0.03 mg/kg i.v.), but not bromocriptine (1 mg/kg i.v.) reduced endogenous 3-MT levels 10 min after administration by approximately 50%. The DA releasing agents d-amphetamine and methylphenidate showed different effects: the former increased endogenous 3-MT greatly, whereas the latter was without effect. The difference is likely to be related to the MAO inhibitory properties of amphetamine. 3-MT disappeared rapidly after COMT inhibition with 50 mg/kg i.v. tropolone (half-life of the initial disappearance about 1 min). The curve flattened off after 5–10 min. Turnover was calculated to be about 7 nmol/g/h, which corresponds to about a third of the turnover of DA. Our results suggest that an important part of DA metabolism occurs through 3-MT and that this amine is very effectively deaminated by MAO-A, so effectively indeed that increased formation does not increase its endogeneous levels. It appears, therefore, that 3-MT is not suitable as an indicator of increased DA release. However, it seems to have some value for an assessment of lowered DA release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00499838
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  • 4
    Electronic Resource
    Electronic Resource
    Further evidence for negative feedback control of serotonin release in the central nervous system (1981)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 317 (1981), S. 36-43 
    Details
    ISSN: 1432-1912
    Keywords: Serotonin ; Cerebral cortex ; Serotonin release ; Serotonin autoreceptors ; Feedback control
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In the presence of the serotonin (5-HT) uptake inhibitor citalopram (2×10−5 M), 5-HT, added to the superfusion medium, diminished the electrically induced 3H-overflow from rat cortex slices prelabelled with 3H-5-HT. A 50% decrease of the 3H-overflow was obtained with 6×10−7 M 5-HT. Of the 5-HT antagonists tested (methysergide, methergoline, methiothepin, cyproheptadine, cinanserin, mianserin, pizotifen), methiothepin (50% at 4.5×10−7 M), methergoline (31% at 10−6 M) and cinanserin (30% at 10−6 M) increased the stimulation-induced 3H-overflow. In some experiments the overflow of endogenous 5-HT was measured simultancously with 3H-overflow. The results were qualitatively and quantitatively very similar, indicating that 3H-overflow can be taken as a reliable measure of 5-HT release. The existence of a functional negative feedback control of 5-HT release mediated by presynaptic autoreceptors was confirmed by analysis of the 3H-overflow per pulse at stimulation frequencies between 0.1 and 50 pulses per second (pps). The 3H-overflow per pulse decreased with increasing stimulus frequency, reaching a low level at 1.6 pps corresponding to 30% of the initial value at 0.1 pps. Methiothepin did not increase the stimulation-induced 3H-overflow at 0.1 pps. The stimulation-induced 5H-overflow at 0.1 pps in the absence of methiothepin was equivalent to that at 1.6 pps in the presence of methiothepin. These results suggest that, under the given experimental conditions, at a stimulation frequency of 0.1 pps the 5-HT concentration in the synaptic cleft drops to very low levels, barely sufficient to induce negative feedback. Among a variety of drugs tested, LSD, dimethyltryptamine, m-chlorophenylpiperazine and clonidine decreased the stimulation-induced 3H-overflow, whereas salbutamol, propranolol, oxprenolol, spiroperidol and haloperidol had no effect. Quipazine, known as a 5-HT agonist, unexpectedly augmented the stimulation-induced 3H-overflow. This effect might be attributable partly to its 5-HT uptake inhibiting component, and also to blockade of presynaptic 5-HT receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00506254
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  • 5
    Electronic Resource
    Electronic Resource
    Serotoninergic modulation of mesolimbic and frontal cortical dopamine neurons (1980)
    Springer
    Cellular and molecular life sciences 36 (1980), S. 1092-1094 
    Details
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Potentiation of the effect of haloperidol on dopamine metabolism by the 5-HT uptake inhibitor CGP 6085 A, and antagonism of this effect by the 5-HT antagonist mianserin were observed in the mesolimbic area and the frontal cortex of the rat brain. A similar effect was reported earlier in the corpus striatum. This suggests that serotoninergic modulation of dopamine neurons is a generally-occurring phenomenon in the brain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01965988
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  • 6
    Electronic Resource
    Electronic Resource
    Urinary excretion of O-methylated catecholamines, tyramine and phenyl-ethylamine by volunteers treated with tranylcypromine and CGP 11305 A (1983)
    Springer
    European journal of clinical pharmacology 25 (1983), S. 361-368 
    Details
    ISSN: 1432-1041
    Keywords: MAO inhibition ; CGP 11305 A ; tranylcypromine ; MAO A ; MAO B ; assessment of MAO inhibition ; urinary catecholamine metabolites ; urinary phenylethylamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary To assess the effect of the new, selective, reversible MAO A inhibitor, CGP 11305 A (4-(5-methoxy-7-bromo-benzofuranyl-2-)piperidine HCl), on MAO A and B activity in man, the daily excretion of total normetanephrine (NMN), metanephrine (MN), 3-methoxytyramine (3-MT) andβ-phenylethylamine (PEA) was measured in the urine of healthy volunteers treated with weekly increasing doses from 40 to 150 mg/d. A similar study was carried out with tranylcypromine in weekly increasing doses from 10 to 25 mg/d. Both compounds increased the excretion of NMN; with CGP 11305 A, a plateau was obtained at 50 mg/d, and tranylcypromine 20 mg was more effective than 10 mg, and was also more active than the highest dose of CGP 11305 A. Increases in MN and 3-MT produced by the latter compound were comparable to that in NMN, whereas tranylcypromine had a biphasic effect on MN excretion, and caused only a small increase in 3-MT excretion. CGP 11305 A up to 150 mg/d did not alter total tyramine excretion, whereas tranylcypromine at 20 mg caused a definite increase. Tranylcypromine led to 4–6 fold increases in PEA output at 20 and 25 mg/d, but not at 10 mg. No such effect could be demonstrated for CGP 11305 A up to 150 mg/d. These results suggest that in man MAO A was inhibited by CGP 11305 A in daily dose of 40 mg or more, whereas it did not affect MAO B at up to 150 mg. Thus, it exhibited considerably greater selectivity than tranylcypromine, which showed only a slight preponderance of inhibition of the A-type enzyme.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01037949
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  • 7
    Electronic Resource
    Electronic Resource
    Supersensitivity to l-5-hydroxytryptophan after 5,7-dihydroxytryptamine injections in desmethylimipramine- and nomifensine-pretreated rats: Behavioral evidence for postsynaptic supersensitivity (1981)
    Springer
    Psychopharmacology 74 (1981), S. 109-114 
    Details
    ISSN: 1432-2072
    Keywords: 5,7 DHT ; Behavioral supersensitivity ; l-5-HTP syndrome ; Serotonin depletion ; Protection of catecholamine neurones
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The behavioral syndrome induced by l-5-hydroxytryptophan (l-5-HTP) in rats was used to study the supersensitivity to l-5-HTP and 5-methoxy-N,N-dimethyltryptamine (5-MeODMT) which develops after unilateral intracerebroventricular (ICV) injections of 200 μg 5,7-dihydroxytryptamine (5,7-DHT). Pretreatment of the animals with a combination of desipramine and nomifensine was found to protect dopamine neurones better than desipramine alone. Maximal behavioral supersensitivity to l-5-HTP and 5-MeODMT was found as early as 24 h after injection of the neurotoxin, even in the presence of the specific 5-HT uptake inhibitor CGP 6085 A, or the MAO-A inhibitor clorgyline. The results indicate that a quickly occurring postsynaptic event contributes to the development of behavioral supersensitivity after ICV injections of 5,7-DHT.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00432674
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  • 8
    Electronic Resource
    Electronic Resource
    Determination of 2-phenylethylamine in rat brain after MAO inhibitors, and in human CSF and urine by capillary GC and chemical ionization MS (1984)
    Springer
    Journal of neural transmission 60 (1984), S. 247-264 
    Details
    ISSN: 1435-1463
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A highly specific and sensitive method for the determination ofβ-phenylethylamine (PEA) in biological material is presented. It involves prepurification of the extracts on Sep-Pak C18 cartridges, derivatization with heptafluorobutyric acid anhydride, gas chromatography on 50 m capillary columns and quantification by chemical ionization mass spectrometry. Using this method, levels of PEA in the rat brain and the effects of various monoamine oxidase (MAO) inhibitors thereon have been determined. PEA control levels were found to vary considerably: the lowest and highest values found were 0.4 and 12.5 ng/g tissue (n=25). Within one and the same control group, the variation was somewhat smaller. The preferential or specific inhibitors of MAO A, amiflamine, cimoxatone, CGP11305 A, moclobemide and toloxatone did not alter rat brain PEA even at high doses. In contrast, the preferential inhibitors of MAO B, deprenil, pargyline and MD 780236, as well as the nonselective agent tranylcypromine, caused strong (up to about 60-fold) increases. The threshold doses corresponded to those which caused about an 80 % inhibition of MAO B as measuredex vivo. The method was also used to determine the concentration of PEA in human CSF (mean 17.3±3.3 ng/ml, range 3–45 ng/ml, n=15) and urine (males: mean 35±5μg/g creatinine, range 3.8–219μg/g, 78 control days of a total of 12 subjects; females: mean 35±6μg/g creat., range 2.7–266μg/g, 55 control days of a total of 8 subjects).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01249097
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  • 9
    Electronic Resource
    Electronic Resource
    The effects of amfonelic acid on 5-HT metabolism in rat brain (1983)
    Springer
    Journal of neural transmission 57 (1983), S. 149-165 
    Details
    ISSN: 1435-1463
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The non-amphetamine stimulant amfonelic acid (AFA), an inhibitor of dopamine (DA) uptake, has been found to increase the levels of tryptophan (TRYP) and 5-hydroxyindoleacetic acid (5-HIAA) in the rat c. striatum, cerebral cortex, and brain stem. Pretreatment with the DA antagonist haloperidol did not affect this action of AFA in the c. striatum, suggesting that it is independent of the effects of this compound on DA neurons. The duration of action of the effect of AFA on TRYP and 5-HIAA appeared to be longer than that of the increase of the striatal DA metabolites homovanillic acid and 3,4-dihydroxyphenylacetic acid. The increased 5-HIAA concentrations seemed only in part be due to a probenecid-like effect of AFA; evidence for an increased 5-HT synthesis, probably related to the increased TRYP concentrations, was also obtained. This biochemical effect of AFA seems to differ from those reported in the literature on amphetamine and other, related stimulating agents. It might be of interest to see whether corresponding behavioural differences between AFA and these agents can be found.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01245115
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