B. Scatton

Sanofi (Turkey)

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Jesús Bénavidès

Instituto de Ciencia y Tecnología de Polímeros

G. Bartholini

Laboratoire de Synthèse Organique

BŽ

B. Živković

National Institute of Mental Health

Dominique Fage

Laboratoire de Synthèse Organique

Y. Claustre

Sanofi (France)

A. Serrano

Laboratoire de Synthèse Organique

A Dubois

Admiraal De Ruyter Ziekenhuis

Kenneth G. Lloyd

Merck & Co., Inc., Rahway, NJ, USA (United States)

Patrick Avenet

Sanofi (France)

Eric T. MacKenzie

Université de Caen Normandie

Cooperative Institutions

Inserm

195

Centre National de la Recherche Scientifique

154

Sanofi (France)

149

Laboratoire de Synthèse Organique

114

Harvard University

Sorbonne Université

University College London

Monash University

Université Paris Cité

University of Pennsylvania

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The NMDA receptor complex

Fundamental and Clinical Pharmacology (1993)

B. Scatton

Summary— The synaptic responses elicited by glutamate and aspartate in the CNS are mediated by distinct groups of receptors which include the ionotropic NMDA receptor. The NMDA receptor is activated by high‐strength synaptic input and produces relatively sustained depolarization which can lead to repetitive burst firing. These characteristics allow it to be involved in the maintainance of rhythmic neuronal activity and in the modulation of synaptic efficacy and plasticity. Overstimulation of the NMDA receptor appears to play a pivotal role in the physiopathology of ischemic brain injury. The NMDA receptor contains an integral cationic channel which is highly permeable to Ca 2+ as well as to Na+ and K+. This receptor has several domains in addition to the NMDA recognition site: i) a divalent cation binding site within the channel pore, at which Mg 2+ ions bind, ii) a binding site recognized by dissociative anesthetics and MK‐801 within the channel; and iii) modulatory sites sensitive to glycine, Zn 2+ and polyamines. The NMDA receptor is strictly controlled by Mg 2+ ions in a voltage‐dependent manner. Moreover, it is modulated by protons, by changes in the redox state and by endogenous physiological substances, eg NO and arachidonic acid. Selective antagonists now exist for the NMDA recognition site and glycine and polyamine modulatory sites. Molecular cloning of the NMDA receptor has identified a subunit termed NMDA‐R1 and four additional subunits (NMDA‐R2A through NMDA‐R2D). Functionally distinct NMDA receptor subtypes are formed by heteromeric assembly of NMDA‐R1 with NMDA‐R2 subunits. NMDA receptor subunits contain consensus phosphorylation sites for protein kinases at the cytoplasmic domain. The high Ca 2+ permeability and sensitivity to channel block by Mg 2+ are imparted by asparagine residues in a putative channel‐forming segment of the protein transmembrane 2. The knowledge of the molecular structure of the NMDA receptor will help to understand the molecular mechanisms responsible for its regulatory features and the molecular bases of neurotoxicity.

10.1111/j.1472-8206.1993.tb01036.x

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Citations (139)

Pharmacological characterisation and autoradiographic distribution of polyamine-sensitive [3H]ifenprodil binding sites in the rat brain

Neuroscience Letters (1991)

Corinne Dana Jesús Bénavidès Hans E. Schoemaker B. Scatton

Ifenprodil

Polyamine

IC50

10.1016/0304-3940(91)90127-f

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Citations (46)

Antagonism by Ng-nitro-l-arginine ofl-glutamate-induced neurotoxicity in cultured neonatal rat cortical neurons. Prolonged application enhances neuroprotective efficacy

Neuroscience (1993)

Xavier Vigé Alexandra Carreau B. Scatton Jean-Pierre Nowicki

Neurotoxicity

Glutamic acid

Nitroarginine

10.1016/0306-4522(93)90306-z

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Citations (49)

Characterization of the excitatory amino acid receptor-mediated release of [3H]acetylcholine from rat striatal slices

Brain Research (1982)

John Lehmann B. Scatton

Kainate receptor

10.1016/0006-8993(82)90980-5

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Citations (157)

Regional pattern of increased ω3 (peripheral type benzodiazepine) binding site densities in the rat brain induced by systemic injection of kainic acid

Neuroscience Letters (1991)

Jesús Bénavidès F. Bourdiol A Dubois B. Scatton

Piriform cortex

Convulsants

10.1016/0304-3940(91)90033-p

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Citations (14)

Presynaptic alpha-2 adrenoceptors play a major role in the effects of idazoxan on cortical noradrenaline release (as measured by in vivo dialysis) in the rat.

Journal of Pharmacology and Experimental Therapeutics (1987)

T Dennis Rémy L'Heureux Christopher Carter B. Scatton

Transcortical dialysis in awake unrestrained rats has been used to evaluate the functional role of differently located alpha-2 adrenoceptors in mediating the action of the alpha-2 adrenoceptor antagonist idazoxan on cerebral noradrenaline release. Basal efflux of noradrenaline collected by a cortically implanted dialysis fiber was stable over a period of 4 days. Systemic injections of idazoxan (20 mg/kg i.p.) increased cortical noradrenaline efflux. This effect was potentiated by pretreatment with the noradrenaline uptake blocker desipramine (20 mg/kg i.p.). Local cortical infusion of (10(-4) M idazoxan which provides a theoretical extracellular administration of 4 to 48 microM) via the dialysis fiber, thus eliminating the potential contribution of somatodendritic alpha-2 adrenoceptors, also elevated cortical noradrenaline efflux. Desipramine (20 mg/kg i.p.) potentiated this effect. Four days after lesioning cortical cell bodies with ibotenic acid (20 min infusion of 10(-4) M ibotenic acid via the dialysis fiber), both systemic injections and local cortical infusions of idazoxan were still effective in increasing cortical noradrenaline efflux. Lesion of serotonergic afferents to the cerebral cortex (by i.c.v. injection of 5,7-dihydroxytryptamine) or of cortical cholinergic afferents (by bilateral electrocoagulation of the nucleus basalis magnocellularis) did not affect the ability of cortical idazoxan infusion to stimulate noradrenaline efflux. The results suggest that the effects of idazoxan on cortical noradrenaline release are mediated primarily by alpha-2 adrenoceptors on noradrenergic nerve terminals, rather than by those located postsynaptically, somatodendritically or on the terminals of other neuronal inputs to the cerebral cortex.

Idazoxan

Desipramine

Ibotenic acid

Nucleus basalis

10.1016/s0022-5347(25)00278-2

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Citations (201)

Interaction of GABA mimetics with nigro-striatal dopamine neurons

Brain Research Bulletin (1980)

Kenneth G. Lloyd P. Worms B. Živković B. Scatton G. Bartholini

Catalepsy

Muscimol

GABA receptor antagonist

Apomorphine

10.1016/0361-9230(80)90070-2

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Citations (18)

Modification of cerebral monoamines in the rat in the course of experimental scrapie

F Cathala L. Court Dominique Fage J. Dedek B. Scatton

Course (navigation)

Source

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Citations (0)

Les stratégies de recherche de nouveaux anti-épileptiques dans le secteur industriel

Epilepsies (2009)

B. Scatton Jean-Michel Stutzmann

Auteur(s) : Bernard Scatton1,2, Jean-Michel Stutzmann1,2 1Departement de recherche Amont, Sanofi-Aventis R&D, 31, avenue Paul-Vaillant-Couturier, 92220 Bagneux (BS), France 2Departement de recherche Amont, Sanofi-Aventis R&D, 13, quai Jules-Guesde, 94403 Vitry-sur-Seine (JMS), France L’epilepsie est une maladie neurologique dont l’incidence (40-80/100 000/an dans les pays developpes incluant 30 % de cas severes ou pharmacoresistants) et la prevalence [...]

10.1684/epi.2009.0252

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Citations (0)

LACK OF EVIDENCE FOR AXONAL TRANSPORT OF D₁ AND D₂ RECEPTORS IN THE NIGRO‐STRIATAL PATHWAY OF THE RAT

Fundamental and Clinical Pharmacology (1988)

Marc Savasta A Dubois B. Scatton

The possibility that D1 and D2 dopamine receptors are axonally transported in the nigro-striatal pathway has been investigated in the rat by placing a coronal knife cut (sparing the striato-nigral pathway) through the medial forebrain bundle (MFB) and autoradiographically examining the density of D2 (as labeled by [3H]spiperone in the presence of ketanserin) and D1 (as labeled by [3H]SCH 23390) receptors. The efficacy of MFB transection has been assessed by measuring in parallel the binding of [3]ketanserin, a ligand that has been reported to be axonally transported in this bundle. At 12 h post-transection, there was a minor accumulation of [3H]spiperone binding on both sides of the transection. However, (+)butaclamol (1 microM) failed to displace the ligand build-up at the knife cut, thus demonstrating the nonspecific nature of [3H]spiperone accumulation. Similar results were observed at 24, 48, and 72 h after severing the MFB. MFB transection also failed to cause changes in specific [3H]SCH 23390 binding at the knife cut at 12-72 h post-surgery. In contrast, a dramatic accumulation of [3H]ketanserin binding sites was observed rostral and caudal to the cut at 12 h post-transection, attesting to the efficacy of the lesion. These results confirm the existence of both anterograde and retrograde transport of [3H]ketanserin binding sites and suggest that D1 and D2 receptors are not axonally transported in fibers of the nigro-striatal pathway.

Ketanserin

Medial forebrain bundle

Spiperone

Axoplasmic transport

10.1111/j.1472-8206.1988.tb00651.x

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Citations (1)