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359 results on '"Nargeot, J."'

25. Cardioprotective effects of chinese medicine NurAiD™II

Author

Vincent, A., primary, Thoumala, S., additional, Covinhes, A., additional, Barrere, C., additional, Gallot, L., additional, Piot, C., additional, Heurteaux, C., additional, Lazdunski, M., additional, Nargeot, J., additional, and Barrere-Lemaire, S., additional

Published
2017
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29. Acetaminophen: a central analgesic drug that involves a spinal tropisetron-sensitive, non-5-HT(3) receptor-mediated effect

Author

Frédéric Libert, Bonnefont J, Bourinet E, Doucet E, Alloui A, Hamon M, Nargeot J, and Eschalier A

Subjects
Male, Analgesics, Indoles, Tropisetron, Biguanides, Oligodeoxyribonucleotides, Antisense, Rats, Spinal Cord, Animals, Serotonin 5-HT3 Receptor Antagonists, Drug Interactions, Serotonin Antagonists, Receptors, Serotonin, 5-HT3, Acetaminophen
Abstract

The reversal of the antinociceptive effect of systemically administered acetaminophen (paracetamol) by intrathecal administration of the potent 5-HT(3) receptor antagonist tropisetron has been reported in rats subjected to the paw pressure test, suggesting that acetaminophen action is mediated through spinal 5-HT(3) receptors. However, more recent data, showing differences between the pharmacological profiles of various 5-HT(3) receptor antagonists, led us to reconsider the involvement of spinal 5-HT(3) receptors. To address this question, two different approaches were used: 1) electrophysiological recordings to assess whether acetaminophen directly modulates 5-HT(3) receptor activity and 2) pharmacological investigations with various 5-HT(3) receptor antagonists and spinal 5-HT(3) receptors antisense oligodeoxynucleotides (AODNs) to determine how those treatments might affect the antinociceptive action of acetaminophen. Electrophysiological studies demonstrated that acetaminophen had no direct agonist or antagonist effects on 5-HT(3A) receptors. Unlike tropisetron, other 5-HT(3) receptor antagonists, such as ondansetron and granisetron, injected intrathecally were unable to reverse the antinociceptive effect of acetaminophen. Moreover, pretreatment with AODNs did not reverse the acetaminophen-induced antinociceptive effect, although it suppressed the antinociceptive effect of m-chlorophenylbiguanide, a specific agonist of 5-HT(3) receptors, and significantly reduced (30%) the expression of these receptors in the dorsal horn of the spinal cord. These results suggest that acetaminophen-induced antinociceptive action involves a spinal tropisetron-sensitive receptor that is not the 5-HT(3) receptor and that remains to be identified.

Published
2004

34. [Molecular genetics of cardiovascular calcium channels]

Author

philippe LORY, Monteil A, and Nargeot J

Subjects
Gene Expression Regulation, Myocardium, Molecular Sequence Data, Mutation, Chromosome Mapping, Genetic Variation, Humans, Muscle Proteins, Calcium Channels, Cloning, Molecular, Recombinant Proteins
Abstract

Cardiac and vascular myocytes exhibit L type calcium channel currents with slightly different properties. The structural bases of this concept of functional diversity of cardiovascular calcium channels are now known. Firstly, there are multiple isoforms of the alpha 1 pore subunit. In addition, the beta subunit should be presented as an endogenous regulator of the calcium channel. Like the alpha 1 subunit, there are many isoforms of this regulatory subunit. A series of recent experiments has changed our understanding of the mechanisms which govern the expression of a functional diversity of calcium channels in the cardiovascular cells. Several pharmacological sites, such as the dihydropyridine, phenylalkylamine and benzothiazepine receptors, have been identified. The recent developments in the field of molecular genetics of the calcium channels are many and open up new perspectives. Mutations within these channels could be the cause of certain cardiovascular genetic diseases.

Published
1997

35. Characterisation of alpha 1A Ba2+, Sr2+ and Ca2+ currents recorded with the ancillary beta 1-4 subunits

Author

Mangoni, Me, Thierry Cens, Dalle, C., Nargeot, J., and Charnet, P.

Subjects
Binding Sites, Patch-Clamp Techniques, Microinjections, Xenopus, Brain, Gene Expression, Rats, Electrophysiology, Kinetics, Barium, Strontium, Oocytes, Animals, Calcium, Calcium Channels, Ion Channel Gating, Plasmids
Abstract

Xenopus oocytes have been injected with different combinations of expression plasmids carrying the rat brain alpha 1A and different beta (beta 1-4) Ca2+ channel subunit cDNAs. Whole-cell Ba2+ and Ca2+ currents were recorded up to seven days after injection. Intra-oocyte injection of BAPTA allowed us to record uncontaminated Ba2+, Sr2+ currents. The alpha 1A calcium channel showed relative current amplitudes according to the sequence: IBa2+ISr2+ICa2+. The ratio ICa2+/IBa2+ was significantly larger when compared to the class C L-type Ca2+ channel (alpha 1C). However, currents flowing through alpha 1A and alpha (1C) subunits saturate for similar Ba2+ concentrations and display the anomalous mole fraction effect in the presence of mixtures of Ba2+ and Ca2+ ions in the external medium. In oocytes expressing the alpha 1A Ca2+ channel subunit, switching from extracellular Ba2+ to Ca2+ also induced a depolarising shift of current-to-voltage relation and the steady-state inactivation curve, and increased the time-to-peak of the current. Inactivation kinetics were poorly affected. Changes in gating and voltage-dependence of activation, but not in the voltage-dependent inactivation, were independent from the coexpressed beta subunit (except with the beta 4 subunit). Our data constitute strong evidence for the existence of differences in intra-pore Ca2+ binding sites between the alpha 1C and alpha 1A subunits, and emphasise the influence of the charge carrier on the modulation of alpha 1A properties by the beta subunits.

Published
1997

38. Acetaminophen: a central analgesic drug that involves a spinal tropisetron-sensitive, non-5-HT(3) receptor-mediated effect.

Author

Libert, F, Bonnefont, Jérôme, Bourinet, E, Doucet, E, Alloui, Abdelkrim, Hamon, Michel, Nargeot, J, Eschalier, Alain, Libert, F, Bonnefont, Jérôme, Bourinet, E, Doucet, E, Alloui, Abdelkrim, Hamon, Michel, Nargeot, J, and Eschalier, Alain

Abstract

The reversal of the antinociceptive effect of systemically administered acetaminophen (paracetamol) by intrathecal administration of the potent 5-HT(3) receptor antagonist tropisetron has been reported in rats subjected to the paw pressure test, suggesting that acetaminophen action is mediated through spinal 5-HT(3) receptors. However, more recent data, showing differences between the pharmacological profiles of various 5-HT(3) receptor antagonists, led us to reconsider the involvement of spinal 5-HT(3) receptors. To address this question, two different approaches were used: 1) electrophysiological recordings to assess whether acetaminophen directly modulates 5-HT(3) receptor activity and 2) pharmacological investigations with various 5-HT(3) receptor antagonists and spinal 5-HT(3) receptors antisense oligodeoxynucleotides (AODNs) to determine how those treatments might affect the antinociceptive action of acetaminophen. Electrophysiological studies demonstrated that acetaminophen had no direct agonist or antagonist effects on 5-HT(3A) receptors. Unlike tropisetron, other 5-HT(3) receptor antagonists, such as ondansetron and granisetron, injected intrathecally were unable to reverse the antinociceptive effect of acetaminophen. Moreover, pretreatment with AODNs did not reverse the acetaminophen-induced antinociceptive effect, although it suppressed the antinociceptive effect of m-chlorophenylbiguanide, a specific agonist of 5-HT(3) receptors, and significantly reduced (30%) the expression of these receptors in the dorsal horn of the spinal cord. These results suggest that acetaminophen-induced antinociceptive action involves a spinal tropisetron-sensitive receptor that is not the 5-HT(3) receptor and that remains to be identified., info:eu-repo/semantics/published

Published
2004

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