The Experts below are selected from a list of 2340 Experts worldwide ranked by ideXlab platform
Mark J. Millan - One of the best experts on this subject based on the ideXlab platform.
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Simultaneous quantification of Serotonin, dopamine and noradrenaline levels in single frontal cortex dialysates of freely-moving rats reveals a complex pattern of reciprocal auto- and heteroreceptor-mediated control of release
Neuroscience, 1998Co-Authors: A. Gobert, J.-m. Rivet, V Audinot, Adrian Newman-tancredi, Laetitia Cistarelli, Mark J. MillanAbstract:Abstract In the present study, a novel and exceptionally sensitive method of high-performance liquid chromatography coupled to coulometric detection, together with concentric dialysis probes, was exploited for an examination of the role of autoreceptors and heteroceptors in the modulation of dopamine, noradrenaline and Serotonin levels in single samples of the frontal cortex of freely-moving rats. The selective D 3 /D 2 receptor agonist, CGS 15855A [(±)- trans -1,3,4,4a,5,10b-hexahydro-4-propyl-2H-[1]benzopyrano[3,4-b]-pyridin-9-ol], and Antagonist, raclopride, respectively decreased (−50%) and increased (+60%) levels of dopamine without significantly modifying those of Serotonin and noradrenaline. The selective α 2 -adrenergic receptor agonist, dexmedetomidine, markedly decreased noradrenaline levels (−100%) and likewise suppressed those of Serotonin and dopamine by −55 and −45%, respectively. This effect was mimicked by the preferential α 2A -adrenergic receptor agonist, guanabenz (−100%, −60% and −50%). Furthermore, the α 2 -adrenergic receptor Antagonist, RX 821,002 [2(2-methoxy-1,4-benzodioxan-2-yl)-2-imidazoline], and the preferential α 2A -adrenergic receptor Antagonist, BRL 44408 [2-(2H-(1-methyl-1,3-dihydroisoindole)methyl)-4,5-dihydroimidazole], both evoked a pronounced elevation in levels of noradrenaline (+212%, +109%) and dopamine (+73%, +85%). In contrast, the preferential α 2B/2C -adrenergic receptor Antagonist, prazosin, did not modify noradrenaline and dopamine levels. RX 821,002 and BRL 44408 did not significantly modify levels of Serotonin, whereas prazosin decreased these levels markedly (−55%), likely due to its α 1 -adrenergic receptor Antagonist properties. The selective Serotonin-1A receptor agonist, 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT), reduced Serotonin levels (−65%) and increased those of dopamine and noradrenaline by +100% and +175%, respectively. The selective Serotonin-1A Antagonist, WAY 100,635 [ N -{2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl}- N -(2-pyridinyl)cyclo-hexanecarboxamide], which had little affect on monoamine levels alone, abolished the influence of 8-OH-DPAT upon Serotonin and dopamine levels and significantly attenuated its influence upon noradrenaline levels. Finally, the selective Serotonin-1B agonist, GR 46611 [3-[3-(2-dimethylaminoethyl)-1H-indol-5-yl]- N -(4-methoxybenzyl)acrylamide], decreased Serotonin levels (−49%) and the Serotonin-1B Antagonist, GR 127,935 [ N -[4-methoxy- 3-(4-methylpiperazin-1-yl)phenyl]-2′-methyl-4′-(5-methyl-1,2,4-oxadiazol-3-yl)-biphenyl-4-carboxamide], which did not significantly modify Serotonin levels alone, abolished this action of GR 46611. Levels of dopamine and noradrenaline were not affected by GR 46611 or GR 127,935. In conclusion, there is a complex pattern of reciprocal autoreceptor and heteroceptor control of monoamine release in the frontal cortex. Most notably, activation of α 2 -adrenergic receptors inhibits the release of noradrenaline, dopamine and Serotonin in each case, while stimulation of Serotonin-1A receptors suppresses Serotonin, yet facilitates noradrenaline and dopamine release. In addition, dopamine D 2 /D 3 autoreceptors restrain dopamine release while (terminal-localized) Serotonin-1B receptors reduce Serotonin release. Control of Serotonin release is expressed phasically and that of noradrenaline and dopamine release tonically.
A. Gobert - One of the best experts on this subject based on the ideXlab platform.
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Simultaneous quantification of Serotonin, dopamine and noradrenaline levels in single frontal cortex dialysates of freely-moving rats reveals a complex pattern of reciprocal auto- and heteroreceptor-mediated control of release
Neuroscience, 1998Co-Authors: A. Gobert, J.-m. Rivet, V Audinot, Adrian Newman-tancredi, Laetitia Cistarelli, Mark J. MillanAbstract:Abstract In the present study, a novel and exceptionally sensitive method of high-performance liquid chromatography coupled to coulometric detection, together with concentric dialysis probes, was exploited for an examination of the role of autoreceptors and heteroceptors in the modulation of dopamine, noradrenaline and Serotonin levels in single samples of the frontal cortex of freely-moving rats. The selective D 3 /D 2 receptor agonist, CGS 15855A [(±)- trans -1,3,4,4a,5,10b-hexahydro-4-propyl-2H-[1]benzopyrano[3,4-b]-pyridin-9-ol], and Antagonist, raclopride, respectively decreased (−50%) and increased (+60%) levels of dopamine without significantly modifying those of Serotonin and noradrenaline. The selective α 2 -adrenergic receptor agonist, dexmedetomidine, markedly decreased noradrenaline levels (−100%) and likewise suppressed those of Serotonin and dopamine by −55 and −45%, respectively. This effect was mimicked by the preferential α 2A -adrenergic receptor agonist, guanabenz (−100%, −60% and −50%). Furthermore, the α 2 -adrenergic receptor Antagonist, RX 821,002 [2(2-methoxy-1,4-benzodioxan-2-yl)-2-imidazoline], and the preferential α 2A -adrenergic receptor Antagonist, BRL 44408 [2-(2H-(1-methyl-1,3-dihydroisoindole)methyl)-4,5-dihydroimidazole], both evoked a pronounced elevation in levels of noradrenaline (+212%, +109%) and dopamine (+73%, +85%). In contrast, the preferential α 2B/2C -adrenergic receptor Antagonist, prazosin, did not modify noradrenaline and dopamine levels. RX 821,002 and BRL 44408 did not significantly modify levels of Serotonin, whereas prazosin decreased these levels markedly (−55%), likely due to its α 1 -adrenergic receptor Antagonist properties. The selective Serotonin-1A receptor agonist, 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT), reduced Serotonin levels (−65%) and increased those of dopamine and noradrenaline by +100% and +175%, respectively. The selective Serotonin-1A Antagonist, WAY 100,635 [ N -{2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl}- N -(2-pyridinyl)cyclo-hexanecarboxamide], which had little affect on monoamine levels alone, abolished the influence of 8-OH-DPAT upon Serotonin and dopamine levels and significantly attenuated its influence upon noradrenaline levels. Finally, the selective Serotonin-1B agonist, GR 46611 [3-[3-(2-dimethylaminoethyl)-1H-indol-5-yl]- N -(4-methoxybenzyl)acrylamide], decreased Serotonin levels (−49%) and the Serotonin-1B Antagonist, GR 127,935 [ N -[4-methoxy- 3-(4-methylpiperazin-1-yl)phenyl]-2′-methyl-4′-(5-methyl-1,2,4-oxadiazol-3-yl)-biphenyl-4-carboxamide], which did not significantly modify Serotonin levels alone, abolished this action of GR 46611. Levels of dopamine and noradrenaline were not affected by GR 46611 or GR 127,935. In conclusion, there is a complex pattern of reciprocal autoreceptor and heteroceptor control of monoamine release in the frontal cortex. Most notably, activation of α 2 -adrenergic receptors inhibits the release of noradrenaline, dopamine and Serotonin in each case, while stimulation of Serotonin-1A receptors suppresses Serotonin, yet facilitates noradrenaline and dopamine release. In addition, dopamine D 2 /D 3 autoreceptors restrain dopamine release while (terminal-localized) Serotonin-1B receptors reduce Serotonin release. Control of Serotonin release is expressed phasically and that of noradrenaline and dopamine release tonically.
J.-m. Rivet - One of the best experts on this subject based on the ideXlab platform.
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Simultaneous quantification of Serotonin, dopamine and noradrenaline levels in single frontal cortex dialysates of freely-moving rats reveals a complex pattern of reciprocal auto- and heteroreceptor-mediated control of release
Neuroscience, 1998Co-Authors: A. Gobert, J.-m. Rivet, V Audinot, Adrian Newman-tancredi, Laetitia Cistarelli, Mark J. MillanAbstract:Abstract In the present study, a novel and exceptionally sensitive method of high-performance liquid chromatography coupled to coulometric detection, together with concentric dialysis probes, was exploited for an examination of the role of autoreceptors and heteroceptors in the modulation of dopamine, noradrenaline and Serotonin levels in single samples of the frontal cortex of freely-moving rats. The selective D 3 /D 2 receptor agonist, CGS 15855A [(±)- trans -1,3,4,4a,5,10b-hexahydro-4-propyl-2H-[1]benzopyrano[3,4-b]-pyridin-9-ol], and Antagonist, raclopride, respectively decreased (−50%) and increased (+60%) levels of dopamine without significantly modifying those of Serotonin and noradrenaline. The selective α 2 -adrenergic receptor agonist, dexmedetomidine, markedly decreased noradrenaline levels (−100%) and likewise suppressed those of Serotonin and dopamine by −55 and −45%, respectively. This effect was mimicked by the preferential α 2A -adrenergic receptor agonist, guanabenz (−100%, −60% and −50%). Furthermore, the α 2 -adrenergic receptor Antagonist, RX 821,002 [2(2-methoxy-1,4-benzodioxan-2-yl)-2-imidazoline], and the preferential α 2A -adrenergic receptor Antagonist, BRL 44408 [2-(2H-(1-methyl-1,3-dihydroisoindole)methyl)-4,5-dihydroimidazole], both evoked a pronounced elevation in levels of noradrenaline (+212%, +109%) and dopamine (+73%, +85%). In contrast, the preferential α 2B/2C -adrenergic receptor Antagonist, prazosin, did not modify noradrenaline and dopamine levels. RX 821,002 and BRL 44408 did not significantly modify levels of Serotonin, whereas prazosin decreased these levels markedly (−55%), likely due to its α 1 -adrenergic receptor Antagonist properties. The selective Serotonin-1A receptor agonist, 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT), reduced Serotonin levels (−65%) and increased those of dopamine and noradrenaline by +100% and +175%, respectively. The selective Serotonin-1A Antagonist, WAY 100,635 [ N -{2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl}- N -(2-pyridinyl)cyclo-hexanecarboxamide], which had little affect on monoamine levels alone, abolished the influence of 8-OH-DPAT upon Serotonin and dopamine levels and significantly attenuated its influence upon noradrenaline levels. Finally, the selective Serotonin-1B agonist, GR 46611 [3-[3-(2-dimethylaminoethyl)-1H-indol-5-yl]- N -(4-methoxybenzyl)acrylamide], decreased Serotonin levels (−49%) and the Serotonin-1B Antagonist, GR 127,935 [ N -[4-methoxy- 3-(4-methylpiperazin-1-yl)phenyl]-2′-methyl-4′-(5-methyl-1,2,4-oxadiazol-3-yl)-biphenyl-4-carboxamide], which did not significantly modify Serotonin levels alone, abolished this action of GR 46611. Levels of dopamine and noradrenaline were not affected by GR 46611 or GR 127,935. In conclusion, there is a complex pattern of reciprocal autoreceptor and heteroceptor control of monoamine release in the frontal cortex. Most notably, activation of α 2 -adrenergic receptors inhibits the release of noradrenaline, dopamine and Serotonin in each case, while stimulation of Serotonin-1A receptors suppresses Serotonin, yet facilitates noradrenaline and dopamine release. In addition, dopamine D 2 /D 3 autoreceptors restrain dopamine release while (terminal-localized) Serotonin-1B receptors reduce Serotonin release. Control of Serotonin release is expressed phasically and that of noradrenaline and dopamine release tonically.
V Audinot - One of the best experts on this subject based on the ideXlab platform.
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Simultaneous quantification of Serotonin, dopamine and noradrenaline levels in single frontal cortex dialysates of freely-moving rats reveals a complex pattern of reciprocal auto- and heteroreceptor-mediated control of release
Neuroscience, 1998Co-Authors: A. Gobert, J.-m. Rivet, V Audinot, Adrian Newman-tancredi, Laetitia Cistarelli, Mark J. MillanAbstract:Abstract In the present study, a novel and exceptionally sensitive method of high-performance liquid chromatography coupled to coulometric detection, together with concentric dialysis probes, was exploited for an examination of the role of autoreceptors and heteroceptors in the modulation of dopamine, noradrenaline and Serotonin levels in single samples of the frontal cortex of freely-moving rats. The selective D 3 /D 2 receptor agonist, CGS 15855A [(±)- trans -1,3,4,4a,5,10b-hexahydro-4-propyl-2H-[1]benzopyrano[3,4-b]-pyridin-9-ol], and Antagonist, raclopride, respectively decreased (−50%) and increased (+60%) levels of dopamine without significantly modifying those of Serotonin and noradrenaline. The selective α 2 -adrenergic receptor agonist, dexmedetomidine, markedly decreased noradrenaline levels (−100%) and likewise suppressed those of Serotonin and dopamine by −55 and −45%, respectively. This effect was mimicked by the preferential α 2A -adrenergic receptor agonist, guanabenz (−100%, −60% and −50%). Furthermore, the α 2 -adrenergic receptor Antagonist, RX 821,002 [2(2-methoxy-1,4-benzodioxan-2-yl)-2-imidazoline], and the preferential α 2A -adrenergic receptor Antagonist, BRL 44408 [2-(2H-(1-methyl-1,3-dihydroisoindole)methyl)-4,5-dihydroimidazole], both evoked a pronounced elevation in levels of noradrenaline (+212%, +109%) and dopamine (+73%, +85%). In contrast, the preferential α 2B/2C -adrenergic receptor Antagonist, prazosin, did not modify noradrenaline and dopamine levels. RX 821,002 and BRL 44408 did not significantly modify levels of Serotonin, whereas prazosin decreased these levels markedly (−55%), likely due to its α 1 -adrenergic receptor Antagonist properties. The selective Serotonin-1A receptor agonist, 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT), reduced Serotonin levels (−65%) and increased those of dopamine and noradrenaline by +100% and +175%, respectively. The selective Serotonin-1A Antagonist, WAY 100,635 [ N -{2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl}- N -(2-pyridinyl)cyclo-hexanecarboxamide], which had little affect on monoamine levels alone, abolished the influence of 8-OH-DPAT upon Serotonin and dopamine levels and significantly attenuated its influence upon noradrenaline levels. Finally, the selective Serotonin-1B agonist, GR 46611 [3-[3-(2-dimethylaminoethyl)-1H-indol-5-yl]- N -(4-methoxybenzyl)acrylamide], decreased Serotonin levels (−49%) and the Serotonin-1B Antagonist, GR 127,935 [ N -[4-methoxy- 3-(4-methylpiperazin-1-yl)phenyl]-2′-methyl-4′-(5-methyl-1,2,4-oxadiazol-3-yl)-biphenyl-4-carboxamide], which did not significantly modify Serotonin levels alone, abolished this action of GR 46611. Levels of dopamine and noradrenaline were not affected by GR 46611 or GR 127,935. In conclusion, there is a complex pattern of reciprocal autoreceptor and heteroceptor control of monoamine release in the frontal cortex. Most notably, activation of α 2 -adrenergic receptors inhibits the release of noradrenaline, dopamine and Serotonin in each case, while stimulation of Serotonin-1A receptors suppresses Serotonin, yet facilitates noradrenaline and dopamine release. In addition, dopamine D 2 /D 3 autoreceptors restrain dopamine release while (terminal-localized) Serotonin-1B receptors reduce Serotonin release. Control of Serotonin release is expressed phasically and that of noradrenaline and dopamine release tonically.
Adrian Newman-tancredi - One of the best experts on this subject based on the ideXlab platform.
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Simultaneous quantification of Serotonin, dopamine and noradrenaline levels in single frontal cortex dialysates of freely-moving rats reveals a complex pattern of reciprocal auto- and heteroreceptor-mediated control of release
Neuroscience, 1998Co-Authors: A. Gobert, J.-m. Rivet, V Audinot, Adrian Newman-tancredi, Laetitia Cistarelli, Mark J. MillanAbstract:Abstract In the present study, a novel and exceptionally sensitive method of high-performance liquid chromatography coupled to coulometric detection, together with concentric dialysis probes, was exploited for an examination of the role of autoreceptors and heteroceptors in the modulation of dopamine, noradrenaline and Serotonin levels in single samples of the frontal cortex of freely-moving rats. The selective D 3 /D 2 receptor agonist, CGS 15855A [(±)- trans -1,3,4,4a,5,10b-hexahydro-4-propyl-2H-[1]benzopyrano[3,4-b]-pyridin-9-ol], and Antagonist, raclopride, respectively decreased (−50%) and increased (+60%) levels of dopamine without significantly modifying those of Serotonin and noradrenaline. The selective α 2 -adrenergic receptor agonist, dexmedetomidine, markedly decreased noradrenaline levels (−100%) and likewise suppressed those of Serotonin and dopamine by −55 and −45%, respectively. This effect was mimicked by the preferential α 2A -adrenergic receptor agonist, guanabenz (−100%, −60% and −50%). Furthermore, the α 2 -adrenergic receptor Antagonist, RX 821,002 [2(2-methoxy-1,4-benzodioxan-2-yl)-2-imidazoline], and the preferential α 2A -adrenergic receptor Antagonist, BRL 44408 [2-(2H-(1-methyl-1,3-dihydroisoindole)methyl)-4,5-dihydroimidazole], both evoked a pronounced elevation in levels of noradrenaline (+212%, +109%) and dopamine (+73%, +85%). In contrast, the preferential α 2B/2C -adrenergic receptor Antagonist, prazosin, did not modify noradrenaline and dopamine levels. RX 821,002 and BRL 44408 did not significantly modify levels of Serotonin, whereas prazosin decreased these levels markedly (−55%), likely due to its α 1 -adrenergic receptor Antagonist properties. The selective Serotonin-1A receptor agonist, 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT), reduced Serotonin levels (−65%) and increased those of dopamine and noradrenaline by +100% and +175%, respectively. The selective Serotonin-1A Antagonist, WAY 100,635 [ N -{2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl}- N -(2-pyridinyl)cyclo-hexanecarboxamide], which had little affect on monoamine levels alone, abolished the influence of 8-OH-DPAT upon Serotonin and dopamine levels and significantly attenuated its influence upon noradrenaline levels. Finally, the selective Serotonin-1B agonist, GR 46611 [3-[3-(2-dimethylaminoethyl)-1H-indol-5-yl]- N -(4-methoxybenzyl)acrylamide], decreased Serotonin levels (−49%) and the Serotonin-1B Antagonist, GR 127,935 [ N -[4-methoxy- 3-(4-methylpiperazin-1-yl)phenyl]-2′-methyl-4′-(5-methyl-1,2,4-oxadiazol-3-yl)-biphenyl-4-carboxamide], which did not significantly modify Serotonin levels alone, abolished this action of GR 46611. Levels of dopamine and noradrenaline were not affected by GR 46611 or GR 127,935. In conclusion, there is a complex pattern of reciprocal autoreceptor and heteroceptor control of monoamine release in the frontal cortex. Most notably, activation of α 2 -adrenergic receptors inhibits the release of noradrenaline, dopamine and Serotonin in each case, while stimulation of Serotonin-1A receptors suppresses Serotonin, yet facilitates noradrenaline and dopamine release. In addition, dopamine D 2 /D 3 autoreceptors restrain dopamine release while (terminal-localized) Serotonin-1B receptors reduce Serotonin release. Control of Serotonin release is expressed phasically and that of noradrenaline and dopamine release tonically.
