M.B. Assié

Pierre Fabre (France)

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Adrian Newman‐Tancredi

Neurolixis (United States)

Cristina Cosi

Instituto de Salud Carlos III

Elisabeth Carilla-Durand

Pierre Fabre (France)

Mike Briley

The University of Texas at Austin

Wouter Koek

The University of Texas Health Science Center at San Antonio

Laurent Bardin

Pierre Fabre (France)

Christiane Palmier

Pierre Fabre (France)

L. Bruins Slot

Pierre Fabre (France)

Ronan Depoortère

Pierre Fabre (France)

Didier Cussac

Laboratoire de Biologie Moléculaire de la Cellule

Cooperative Institutions

Pierre Fabre (France)

Pierre Fabre (Germany)

Inserm

Centre National de la Recherche Scientifique

Centro de Investigación Biomédica en Red de Salud Mental

Consorci Institut D'Investigacions Biomediques August Pi I Sunyer

Institut d'Investigacions Biomèdiques de Barcelona

Instituto de Salud Carlos III

Consejo Superior de Investigaciones Científicas

Centro de Investigación Biomédica en Red

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Differential in vivo Inhibition of [<sup>3</sup>H]Nemonapride Binding by Atypical Antipsychotics in Rat Striatum, Olfactory Lobes, and Frontal Cortex

Pharmacology (2005)

M.B. Assié N. Consul-Denjean Wouter Koek Adrian Newman‐Tancredi

Dopamine D2 receptor blockade is thought to be mandatory for antipsychotic action because most of the currently used antipsychotics have high affinity at these receptors. Here, we examined the in vivo binding characteristics of the D2-like receptor antagonist [3H]nemonapride in rat brain areas including the striatum, olfactory lobes and frontal cortex and its inhibition by a series of D2 antagonist antipsychotics. In vivo affinity of [3H]nemonapride was similar (apparent Kd value: 0.05 micromol/kg) in all brain regions examined. The estimated number of binding sites was higher in the striatum (66 fmol/mg wet weight) than in the olfactory lobes (28 fmol/mg wet weight) and the frontal cortex (21 fmol/mg wet weight). In the striatum, [3H]nemonapride binding was inhibited in a dose-dependent manner with the following order of potency (ED50, mg/kg): nemonapride (0.04), raclopride (0.13), spiperone and risperidone (0.14), haloperidol (0.21), clozapine (7.2) and thioridazine (9.4); in the olfactory lobes: nemonapride (0.03), raclopride and spiperone (0.09), haloperidol (0.10), risperidone (0.15), thioridazine and clozapine (11); in the frontal cortex, only the high affinity dopamine D2 antagonist compounds nemonapride (0.05), haloperidol (0.09), and raclopride (0.12) significantly decreased the binding of [3H]nemonapride. The present data suggest that conventional and atypical antipsychotics may be distinguished by their differential occupancy of striatal versus frontocortical D2-like receptors in vivo.

Raclopride

Dopamine antagonist

Ventral striatum

10.1159/000086948

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Citations (7)

P.1.c.047 F15599, a post-synaptic cortical preferential 5-HT1A agonist: III) electrophysiology and microdialysis

European Neuropsychopharmacology (2008)

Laia Lladó-Pelfort M.B. Assié Pau Celada Adrian Newman‐Tancredi Francesc Artigas

Pindolol

5-HT1A receptor

Ketanserin