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  • 1
    Electronic Resource
    Electronic Resource
    Sustained Dopamine Release Induced by Secretoneurin in the Striatum of the Rat: A Microdialysis Study (1995)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 65 (1995), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Secretoneurin (SN) is a neuropeptide derived from secretogranin II that is found in brain and endocrine tissues. The aim of the present study was to determine the influence of this novel peptide on dopamine (DA) release from rat striatum using the microdialysis technique. Rat SN (1–30 µmol/L added to the dialysis buffer) enhanced DA outflow of awake rats in a concentration-dependent way without marked effects on the outflow of 3,4-dihydroxyphenylacetic acid or homovanillic acid. The increase in extracellular DA content caused by the peptide was observed throughout the entire period of administration (up to 4 h). Human SN and its 15-amino-acid C-terminal sequence also increased DA outflow, but the effects were smaller than those of rat SN. Two other peptides derived from secretogranin II were without effect on DA efflux. These results establish that SN has a pronounced effect on DA release under in vivo conditions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1995.65020622.x
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  • 2
    Electronic Resource
    Electronic Resource
    Carrier-Mediated Release, Transport Rates, and Charge Transfer Induced by Amphetamine, Tyramine, and Dopamine in Mammalian Cells Transfected with the Human Dopamine Transporter (1998)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 71 (1998), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Amphetamine and related substances induce dopamine release. According to a traditional explanation, this dopamine release occurs in exchange for amphetamine by means of the dopamine transporter (DAT). We tested this hypothesis in human embryonic kidney 293 cells stably transfected with the human DAT by measuring the uptake of dopamine, tyramine, and d- and l-amphetamine as well as substrate-induced release of preloaded N-methyl-4-[3H]phenylpyridinium ([3H]MPP+). The uptake of substrates was sodium-dependent and was inhibited by ouabain and cocaine, which also prevented substrate-induced release of MPP+. Patch-clamp recordings revealed that all four substrates elicited voltage-dependent inward currents (on top of constitutive leak currents) that were prevented by cocaine. Whereas individual substrates had similar affinities in release, uptake, and patch-clamp experiments, maximal effects displayed remarkable differences. Hence, maximal effects in release and current induction were ∼25% higher for d-amphetamine as compared with the other substrates. By contrast, dopamine was the most efficacious substrate in uptake experiments, with its maximal initial uptake rate exceeding those of amphetamine and tyramine by factors of 20 and 4, respectively. Our experiments indicate a poor correlation between substrate-induced release and the transport of substrates, whereas the ability of substrates to induce currents correlates well with their releasing action.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1998.71031289.x
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  • 3
    Electronic Resource
    Electronic Resource
    Pulse-to-Pulse Modulation of Transmitter Release in the Central Nervous System Basic and Pharmacological Aspects (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 604 (1990), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1990.tb31995.x
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  • 4
    Electronic Resource
    Electronic Resource
    ELEVATION OF NEUROTENSIN IN THE CENTRAL REGULATION OF LUTEINIZING HORMONE RELEASE (1982)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 400 (1982), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1982.tb31584.x
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  • 5
    Electronic Resource
    Electronic Resource
    B-HT 920 and B-HT 958: Presynaptic effects on electrically evoked 3H-dopamine release from slices of rat nucleus accumbens (1987)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 335 (1987), S. 28-31 
    Details
    ISSN: 1432-1912
    Keywords: B-HT 920 ; B-HT 958 ; Presynaptic dopamine autoreceptors ; Dopamine release ; Nucleus accumbens
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of two thiazoloazepine derivatives, B-HT 920 (6-allyl-2-amino-5,6,7,8-tetrahydro-4H-thiazolo[4,5-d]azepine) and B-HT 958 (2-amino-6-(p-chloro-benzyl)-4H-5,6,7,8-tetrahydrothiazolo[5,4-d]azepine) on electrically evoked overflow of 3H-dopamine were studied. Slices from nucleus accumbens of the rat were preincubated with 3H-dopamine and superfused at 23°C or 37°C. Electrical field stimulation was applied using frequencies of 0.5 or 5 Hz. 1. At 37°C/5 Hz, B-HT 920 markedly and dose-dependently (0.01–0.1 μmol/l) reduced the stimulation evoked overflow of tritium. Its dose-response curve was shifted to the right at 23°C/0.5 Hz and 23°C/5 Hz, respectively. A similar result was obtained with the dopamine receptor agonist, apomorphine (1 μmol/l). 2. B-HT 958 (0.1–10 μmol/l) also reduced electrically induced overflow of tritium at 37°C/5 Hz, had no effect at 23°C/0.5 Hz, and facilitated tritium overflow at 23°C/5 Hz. 3. Sulpiride (10 μmol/l) completely prevented the effects of B-HT 920 (1 μmol/l) or B-HT 958 (1 μmol/l) at 37°C/ 5 Hz, whereas phentolamine (1 μmol/l) had no effect on the actions of the two drugs under these experimental conditions. 4. From the patterns of effects obtained under the different experimental conditions it is concluded that B-HT 920 acts as full agonist at presynaptic dopamine autoreceptors whereas B-HT 958 acts as partial agonist.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00165031
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  • 6
    Electronic Resource
    Electronic Resource
    B-HT 920, B-HT 933, and B-HT 958: presynaptic effects on electrically evoked 3H-noradrenaline release from slices of rat brain cortex and hypothalamus (1987)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 335 (1987), S. 613-617 
    Details
    ISSN: 1432-1912
    Keywords: B-HT 920 ; B-HT 933 ; B-HT 958 ; Presynaptic α2-auto-receptor ; Noradrenaline release
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of the three azepine compounds, B-HT 920 (6-allyl-2-amino-5,6,7,8-tetrahydro-4H-thiazolo-[4,5-d]azepine), B-HT 933 [2-amino-6-ethyl-5, 6, 7, 8-tetrahydro-4H-oxazolo [4,5-d]azepine; azepexole] and B-HT 958 (2-amino-6-(p-chloro-benzyl)-4H-5, 6, 7, 8-tetrahydrothiazolo[5,4-d]azepine) on electrically evoked overflow of 3H-noradrenaline were studied. Slices from parietal cortex (Cξ) or nucleus anterior hypothalami (nah) were incubated with 3H-noradrenaline, superfused at 23°C or 37°C in the presence of the noradrenaline uptake inhibitor desipramine (3 μmol/l) and field stimulated at frequencies of 0.3 or 3 Hz. 1. At 37°C/0.3 Hz, B-HT 920 and B-HT 933 concentration-dependently decreased the evoked overflow of tritium in both regions studied, whereas B-HT 958 had no effect. 2. In a second set of experiments each drug was tested under three additional experimental conditions, i. e. 37°C/3 Hz, 23°C/ 0.3 Hz and 23°C/3 Hz. Increasing the stimulation frequency to 3 Hz or lowering the superfusion temperature to 23°C reduced the effects of B-HT 920 (1 μmol/l) and B-HT 933 (10 μmol/l) as compared to the effects at 37°C/0.3 Hz. When tested at 23°C/3 Hz, both drugs did not significantly affect the evoked overflow of tritium in the Cx or the nah. In contrast, B-HT 958 (10 μmol/l), caused a facilitation of evoked overflow in both regions when the higher stimulation frequency or the lower superfusion temperature was used. Its release-enhancing action was most pronounced at 23°C/3 Hz. 3. Idazoxan (0.1 μmol/l) antagonized the effects of BHT 920 (10 μmol/l) and B-HT 933 (10 gmmol/l) in the Cx at 37°C/0.3 Hz. The ineffectiveness of B-HT 958 under these experimental conditions was not changed in the presence of idazoxan. Sulpiride (10 μmol/l) did not affect the action of any of the three compounds. 4. From the patterns of effects obtained under the different experimental conditions it is concluded that B-HT 920 and B-HT 933 act as agonists at prejunctional α2-adrenoceptors, whereas B-HT 958 acts as a weak antagonist at these sites. Send offprint requests to E. A. Singer at the above address
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00166976
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  • 7
    Electronic Resource
    Electronic Resource
    Evidence against a functional link between noradrenaline uptake mechanisms and presynaptic alpha-2 adrenoceptors (1988)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 337 (1988), S. 118-121 
    Details
    ISSN: 1432-1912
    Keywords: Presynaptic receptors ; α2-Adrenoceptors ; Noradrenaline release
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Slices prepared from rat cerebral cortex were labelled with 3H-noradrenaline and superfused. Electrical field stimulation was carried out 15 min (S1) and 45 min (S2) after the start of collection of 5-min samples using 4 pulses delivered at 100 Hz. Drugs acting at α2-adrenoceptors were added 20 min before S2, and their effects were evaluated using the S2/S1-ratio. The α2-adrenoceptor antagonists idazoxan (1 μmol/l) and rauwolscine (1 μmol/l) failed to increase stimulation-evoked overflow of radioactivity in the absence or presence of the noradrenaline reuptake inhibitor desipramine (1 gmol/l). This indicates that the duration of electrical stimulation was too short to allow development of α2-adrenoceptor-mediated auto-inhibition by released noradrenaline. The effect of clonidine (3–1000 nmol/l) on stimulation-evoked overflow of radioactivity was tested in the absence and presence of three different reuptake inhibitors (desipramine, 1 μol/l; maprotiline, 1 μol/l; cocaine, 10 μmol/l). The analysis yielded identical concentration-response curves under all conditions. These results argue against an action of inhibitors of neuronal reuptake of noradrenaline at the presynaptic α2-adrenoceptor and against the concept of a functional link between uptake site and receptor.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169488
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  • 8
    Electronic Resource
    Electronic Resource
    Effects of clonidine on the stimulation-evoked release of3H-noradrenaline from superfused rat brain slices as a function of the biophase concentration (1986)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 333 (1986), S. 36-42 
    Details
    ISSN: 1432-1912
    Keywords: Noradrenaline release ; Presynaptic α-adrenoceptor ; α2-Adrenoceptor ; Clonidine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The influence of clonidine on the stimulation-evoked overflow of tritium was studied in brain slices preincubated with3H-noradrenaline. The slices were prepared from parietal cortex (Cx), nucleus anterior hypothalami (nah) and nucleus tractus solitarii (nts). After preincubation, the tissues were superfused at 23°C or 37°C with a medium containing the noradrenaline uptake inhibitor desipramine. Electrical field stimulation was applied using stimulation frequencies of 0.3–10 Hz. 1. At 23°C/0.3 Hz, clonidine concentration-dependently inhibited the evoked overflow of tritium in all three brain regions. In contrast, at 23°C/3 Hz the inhibitory effect of the drug in the Cx was abolished and a facilitation was observed in the nah and nts. When tested at increasing frequencies of stimulation in the nts at 23°C, clonidine exerted a dual action, characterized by a reduction of electrically evoked responses at frequencies below 1 Hz and a facilitation at frequencies above 1 Hz. 2. At 37°C, clonidine concentration-dependently decreased the evoked overflow in all brain regions studied, this effect being more pronounced at 0.3 Hz than at 3 Hz. 3. The apparent lack of an effect of clonidine on the stimulation-evoked overflow of tritium in the Cx at 23°C/3 Hz was turned to a facilitation when noradrenaline (0.01 μmol/l) was included in the superfusion medium. Conversely, an inhibitory effect of clonidine was seen when the uptake blocker desipramine (as well as noradrenaline) was omitted from the superfusion medium. 4. The facilitation by clonidine of the stimulus-induced release in the nah at 23°C/3 Hz was reversed to inhibition when the noradrenaline content of the slices was reduced to about 60% by exposure to a medium containing 50 mmol/l potassium before preincubation with3H-noradrenaline. 5. A marked difference regarding the two superfusion temperatures was noted at the ultrastructural level: the superfusion of slices resulted in a widening of extracellular spaces, dissociation of synaptic clefts with preservation of presynaptic terminals, and intracytoplasmatic uptake of horseradish peroxidase. These changes were more pronounced after superfusion at 37°C than at 23°C. In accordance with these observations, the retention of3H-polyethyleneglycol in slices superfused at 37°C was greater than in slices superfused at 23°C. 6. It is concluded that in superfusion/stimulation experiments with brain slices temperature-dependent changes at the ultrastructural level may have an influence on the concentration of noradrenaline in the synaptic cleft. The results emphasize the role of the biophase concentration of noradrenaline with regard to the magnitude and the direction of the presynaptic effect of clonidine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00569657
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  • 9
    Electronic Resource
    Electronic Resource
    Serotonin uptake blockers influence serotonin autoreceptors by increasing the biophase concentration of serotonin and not through a “molecular link” (1990)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 342 (1990), S. 363-370 
    Details
    ISSN: 1432-1912
    Keywords: Rabbit brain cortex ; Rat hypothalamus ; Serotonin release ; Presynaptic serotonin autoreceptors ; Serotonin uptake
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The mechanism of the attenuation, by serotonin uptake blockers, of the release-inhibiting effect of exogenous serotonin autoreceptor agonists was studied in rabbit brain cortex and rat hypothalamus slices. The slices were preincubated with 3H-serotonin and then superfused and stimulated electrically. In rabbit brain slices stimulated by trains of 4 pulses at 100 Hz, 5-carboxamidotryptamine and 5-methoxytryptamine reduced the evoked overflow of tritium, and their concentration-response curves were not changed by any of three serotonin uptake inhibitors, namely citalopram, fluvoxamine and 6-nitroquipazine. In contrast, when the slices were stimulated by trains of 10 pulses at 0.033 Hz, fluvoxamine shifted the concentration-response curve of 5-methoxytryptamine to the right. Experiments with the autoreceptor antagonist metitepine indicated that little, if any, endogenous autoinhibitory tone developed in the course of trains of 4 pulses/100 Hz, irrespective of the absence or presence of uptake inhibitors, as well as during trains of 10 pulses/0.033 Hz in the absence of uptake inhibitors, whereas marked autoinhibition developed when 10 pulses/0.033 Hz were applied in the presence of fluvoxamine. In rat hypothalamic slices stimulated by trains of 4 pulses at 100 Hz, citalopram also failed to change the concentration-response curve of 5-methoxytryptamine. These results indicate that serotonin uptake blockers attenuate the effect of exogenous autoreceptor agonists by an increase in the biophase concentration of released serotonin and, hence, in endogenous autoinhibitory tone, and not by some direct “molecular link” unrelated to the biophase concentration of released serotonin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169450
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  • 10
    Electronic Resource
    Electronic Resource
    Electrically evoked noradrenaline release from cultured chick sympathetic neurons: modulation via presynaptic α2-adrenoceptors and lack of autoinhibition (1991)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 344 (1991), S. 130-132 
    Details
    ISSN: 1432-1912
    Keywords: Chick sympathetic neurons ; Electrical field stimulation ; Noradrenaline release ; Presynaptic α2-adrenoceptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Sympathetic neurons from twelve day old chick embryos were plated on polystyrol discs and kept in culture for five days. After incubation with 3H-noradrenaline the discs were transferred to small chambers and superfused. Electrical field stimulation (36 pulses at 3 Hz) increased the outflow of tritium. The evoked overflow of tritium was abolished in the absence of extracellular calcium and was diminished by about 90% in the presence of tetrodotoxin (1 μmol/l). The α2-adrenoceptor agonist 5-bromo-6-(2-imidazolin-2-ylamino)quinoxaline (UK-14,304) caused a concentration-dependent decrease in overflow, whereas the α1-adrenoceptor agonist methoxamine was ineffective at up to 1 μmol/l. The concentration-response curve of UK-14,304 was shifted to the right by the α2-adrenoceptor antagonist yohimbine (0.03 μmol/l). Yohimbine on its own caused no significant change. The noradrenaline reuptake inhibitor cocaine (10 μmol/l) caused a small (20%) increase in evoked overflow. The results indicate that cultured chick sympathetic neurons possess release-modulating α2-adrenoceptors and that the electrically induced overflow of transmitter occurs under conditions virtually free of autoinhibition.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00167393
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