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Your search keyword '"Cistarelli L"' showing total 3 results
Start Over Author "Cistarelli L" Topic cerebral cortex
3 results on '"Cistarelli L"'

1. Serotonin(2C) receptors tonically suppress the activity of mesocortical dopaminergic and adrenergic, but not serotonergic, pathways: a combined dialysis and electrophysiological analysis in the rat.

Author

Gobert A, Rivet JM, Lejeune F, Newman-Tancredi A, Adhumeau-Auclair A, Nicolas JP, Cistarelli L, Melon C, and Millan MJ

Subjects
Animals, Corpus Striatum metabolism, Dialysis, Dopamine metabolism, Electrophysiology, Epinephrine metabolism, Extracellular Space metabolism, Frontal Lobe metabolism, Locus Coeruleus cytology, Locus Coeruleus physiology, Male, Neurons physiology, Nucleus Accumbens metabolism, Rats, Rats, Wistar, Receptor, Serotonin, 5-HT2A, Receptor, Serotonin, 5-HT2B, Receptor, Serotonin, 5-HT2C, Receptors, Serotonin metabolism, Serotonin metabolism, Serotonin physiology, Tegmentum Mesencephali cytology, Tegmentum Mesencephali metabolism, Cerebral Cortex physiology, Dopamine physiology, Epinephrine physiology, Receptors, Serotonin physiology
Abstract

The present study evaluated, via a combined electrophysiological and dialysis approach, the potential influence of serotonin (5-HT)(2C) as compared to 5-HT(2A) and 5-HT(2B) receptors on dopaminergic, adrenergic, and serotonergic transmission in frontal cortex (FCX). Whereas the selective 5-HT(2A) antagonist MDL100,907 failed to modify extracellular levels of dopamine (DA), noradrenaline (NA) or 5-HT simultaneously quantified in single dialysate samples of freely-moving rats, the 5-HT(2B)/5-HT(2C) antagonist SB206,553 dose-dependently increased levels of DA and NA without affecting those of 5-HT. This action was attributable to 5-HT(2C) receptor blockade inasmuch as the selective 5-HT(2C) antagonist SB242,084 likewise increased FCX levels of DA and NA, whereas the selective 5-HT(2B) antagonist SB204,741 was ineffective. Further, the preferential 5-HT(2C) receptor agonist Ro60-0175 dose-dependently depressed FCX levels of DA. The suppressive influence of 5-HT(2C) receptors on DA release was also expressed on mesolimbic and nigrostriatal dopaminergic pathways, in that levels of DA in nucleus accumbens and striatum were likewise reduced by Ro60-0175 and elevated, though less markedly, by SB206,553. In line with the above findings, Ro60-0175 dose-dependently decreased the firing rate of ventrotegmental dopaminergic and locus coeruleus (LC) adrenergic perikarya, whereas their activity was dose-dependently enhanced by SB206,553. Furthermore, SB206,553 transformed the firing pattern of ventrotegmental dopaminergic neurons into a burst mode. In contrast to SB206,553, MDL100,907 had little affect on the firing rate of dopaminergic or adrenergic neurons. In conclusion, as compared to 5-HT(2A) and 5-HT(2B) receptors, 5-HT(2C) receptors exert a tonic, suppressive influence on the activity of mesocortical - as well as mesolimbic and nigrostriatal - dopaminergic pathways, likely via indirect actions expressed at the level of their cell bodies. Frontocortical adrenergic, but not serotonergic, transmission is also tonically suppressed by 5-HT(2C) receptors., (Copyright 2000 Wiley-Liss, Inc.)

Published
2000
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2. WAY 100,635 enhances both the 'antidepressant' actions of duloxetine and its influence on dialysate levels of serotonin in frontal cortex.

Author

Millan MJ, Brocco M, Veiga S, Cistarelli L, Melon C, and Gobert A

Subjects
Animals, Cerebral Cortex metabolism, Drug Synergism, Duloxetine Hydrochloride, Frontal Lobe drug effects, Frontal Lobe metabolism, Male, Rats, Rats, Wistar, Antidepressive Agents pharmacology, Cerebral Cortex drug effects, Piperazines pharmacology, Pyridines pharmacology, Serotonin metabolism, Serotonin Antagonists pharmacology, Thiophenes pharmacology
Abstract

The mixed serotonin and noradrenaline reuptake inhibitor, duloxetine, (5.0 mg/kg, s.c.), increased levels of serotonin (220%), dopamine (180%) and noradrenaline (470%) in individual dialysates of frontal cortex of freely moving rats. Its influence on serotonin, but not dopamine or noradrenaline, levels was enhanced by the 5-HT1A receptor antagonist, WAY 100,635 (N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-N-(2-pyridinyl) cyclo-hexanecarboxamide 3HCl) (0.16 mg kg(-1), s.c). In the forced swimming test, although duloxetine was inactive alone, it dose dependently reduced immobility in the presence of WAY 100,635. Thus, blockade of 5-HT1A (auto)receptors selectively facilitates the influence of duloxetine on serotonin levels in the frontal cortex in rats and, in the forced swimming model, enhances its 'antidepressant' properties in parallel.

Published
1998
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3. Functional correlates of dopamine D3 receptor activation in the rat in vivo and their modulation by the selective antagonist, (+)-S 14297: II. Both D2 and 'silent' D3 autoreceptors control synthesis and release in mesolimbic, mesocortical and nigrostriatal pathways

Author

Gobert A, Jm, Rivet, Audinot V, Cistarelli L, Michael Spedding, Vian J, Jl, Peglion, and Mj, Millan

Subjects
Cerebral Cortex, Male, Tetrahydronaphthalenes, Receptors, Dopamine D2, Dopamine, Brain, Olfactory Bulb, Corpus Striatum, Nucleus Accumbens, Rats, Receptors, Dopamine, 2-Naphthylamine, Dopamine Agonists, 3,4-Dihydroxyphenylacetic Acid, Animals, Dopamine Antagonists, Rats, Wistar, Furans
Abstract

The preferential dopamine (DA) D3 versus D2 receptor agonist, (+)-7-OH-DPAT, dose-dependently decreased DA synthesis in the nucleus accumbens, olfactory tubercles, striatum and frontal cortex. This action was potently mimicked by several other high-potency D3 agonists: CGS 15855A, (-)-quinpirole, quinelorane and N-0434. In contrast, piribedil, which displays a mild preference for D2 sites, was less active. Across eight agonists, potency for inhibition of DA synthesis correlated more potently to affinity at D3 (r = .82 +/- .04) than D2 receptors (r = .60 +/- .06, P.05). Correlations were also marked to potency for induction of a further D3-mediated response, hypothermia (r = .93 +/- .02). The novel and selective D3 versus D2 antagonist, (+/-)-S 11556, attenuated the action of (+)-7-OH-DPAT in each structure. This action was shared by its active (+)-eutomer, (+)-S 14297, whereas its inactive (-)-distomer, (-)-S 17777, was ineffective. (+)-S 14297 similarly attenuated the inhibitory action of CGS 15855A and (-)-quinpirole upon DA synthesis, whereas it failed to modify inhibition of striatal DA synthesis by the alpha 2-adrenergic receptor agonist, clonidine. As compared with the D2/D3 receptor antagonist, haloperidol, neither (+/-)-S 11566 nor (+)-S 14297 modified DA turnover upon administration alone. Furthermore, across (nine) antagonists, potency in facilitating DA synthesis more powerfully correlated to affinity at D2 (r = .94 +/- .01) than D3 (r = .73 +/- .01) sites (P.01). Correlations were also marked to potency for induction of catalepsy (r = .91 +/- .01) and prolactin secretion (r = .89 +/- .01) but not for antagonism of (+)-7-OH-DPAT-induced hypothermia (r = .60 +/- .01). In freely moving rats, (+)-7-OH-DPAT dose-dependently reduced dialysate concentrations of DA in the nucleus accumbens and contralateral striatum: this action was potently mimicked by CGS 15855A, but only weakly so by piribedil. (+)-S 14297 markedly attenuated the action of (+)-7-OH-DPAT, whereas (-)-S 17777 was inactive. In contrast, haloperidol completely blocked the action of (+)-7-OH-DPAT. Finally, in distinction to haloperidol, upon administration alone, (+)-S 14297 did not significantly enhance the release of DA. In conclusion, these data suggest that D3 (auto)receptors control synthesis and release of DA in dopaminergic pathways innervating the limbic system, cortex and striatum.(ABSTRACT TRUNCATED AT 400 WORDS)

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