Emmanuel Valjent

Inserm

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Jean‐Antoine Girault

Institut du Fer à Moulin

Denis Hervé

Sorbonne Université

Giuseppe Gangarossa

Université Paris Cité

Emma Puighermanal

Université de Montpellier

Laia Castell

Centre National de la Recherche Scientifique

Dimitri De Bundel

Vrije Universiteit Brussel

Gilberto Fisone

Karolinska Institutet

Laura Cutando

Université de Montpellier

Rafaël Maldonado

Pompeu Fabra University

Paul Greengard

Rockefeller University

Cooperative Institutions

Inserm

272

Centre National de la Recherche Scientifique

254

Université de Montpellier

126

Sorbonne Université

108

Université Paris Cité

Institut de Génomique Fonctionnelle

Université de Bordeaux

Instituto de Salud Carlos III

Centro de Investigación Biomédica en Red

Institut du Fer à Moulin

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Absence of Δ-9-Tetrahydrocannabinol Dysphoric Effects in Dynorphin-Deficient Mice

Journal of Neuroscience (2001)

Andreas Zimmer Emmanuel Valjent Monika König Anne Zimmer Patricia Robledo

The involvement of dynorphin on Δ-9-tetrahydrocannabinol (THC) and morphine responses has been investigated by using mice with a targeted inactivation of the prodynorphin (Pdyn) gene. Dynorphin-deficient mice show specific changes in the behavioral effects of THC, including a reduction of spinal THC analgesia and the absence of THC-induced conditioned place aversion. In contrast, acute and chronic opioid effects were normal. The lack of negative motivational effects of THC in the absence of dynorphin demonstrates that this endogenous opioid peptide mediates the dysphoric effects of marijuana.

Dynorphin

Tetrahydrocannabinol

Endogenous opioid

Dynorphin A

Δ9-tetrahydrocannabinol

10.1523/jneurosci.21-23-09499.2001

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Citations (139)

Review for "Striatal transcriptome changes linked to drug‐induced repetitive behaviors"

Emmanuel Valjent

10.1111/ejn.15116/v1/review1

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Operant training for highly palatable food alters translating mRNA in nucleus accumbens D2 neurons and reveals a modulatory role ofNeurochondrin

bioRxiv (Cold Spring Harbor Laboratory) (2023)

Enrica Montalban Albert Giralt Lieng Taing Yuki Nakamura Assunta Pelosi

Highly palatable food triggers behavioral alterations reminiscent of those induced by addictive drugs. These effects involve the reward system and dopamine neurons, which modulate neurons in the nucleus accumbens (NAc). The molecular mechanisms underlying the effects of highly palatable food on feeding behavior are poorly understood.We studied the effects of 2-week operant conditioning of mice with standard or isocaloric highly palatable food. We investigated the behavioral effects and dendritic spine modifications in the NAc. We compared the translating mRNA in NAc neurons identified by the type of dopamine receptors they express, depending on the type of food and training. We tested the consequences of invalidation of an abundant downregulated gene, Ncdn (Neurochondrin).Operant conditioning for highly palatable food increases motivation for food even in well-fed mice. In control mice, free access to regular or highly palatable food results in increased weight as compared to regular food only. Highly palatable food increases spine density in the NAc. In animals trained for highly palatable food, translating mRNAs are modified in NAc dopamine D2-receptor-expressing neurons, mostly corresponding to striatal projection neurons, but not in those expressing D1-receptors. Knock-out of Ncdn, an abundant down-regulated gene, opposes the conditioning-induced changes in satiety-sensitive feeding behavior and apparent motivation for highly palatable food, suggesting down-regulation may be a compensatory mechanism.Our results emphasize the importance of mRNA alterations D2 striatal projection neurons in the NAc in the behavioral consequences of highly palatable food conditioning and suggest a modulatory contribution of Ncdn downregulation.

10.1101/2023.03.07.531496

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La voie mapk/erk : un substrat neurobiologique de la dependance aux substances toxicomanogenes

Emmanuel Valjent

Le but de ce travail fut de valider un modele permettant l'etude des proprietes motivationnelles induites par le thc chez la souris puis d'evaluer le role de la voie de signalisation mapk/erk dans la mise en place des adaptations neuronales responsables des comportements addictifs du thc et de la cocaine. Les reponses motivationnelles induites par le thc ont ete evaluees dans le test de preference de place, en minimisant les effets dysphoriques induits par la premiere exposition a la drogue et/ou les consequences des proprietes pharmacocinetiques du compose. Ainsi, selon la dose et le protocole experimental utilise, le thc est capable d'induire a la fois des effets renforcants et aversifs. L'administration aigue de cocaine et de thc chez la souris, s'accompagne d'une augmentation transitoire de la phosphorylation des erks dans les cellules striatales. La liberation de dopamine constitue un evenement majeur dans l'activation des erks qui est totalement dependante de la stimulation des recepteurs d1 avec une contribution partielle des recepteurs d2. Les recepteurs nmda interviennent egalement dans l'activation des erks par ces deux substances. L'activation du facteur de transcription elk-1 et la regulation transcriptionnelle des genes precoces c-fos et zif268 en reponse a l'administration aigue de thc et de cocaine sont controlees par les voies erks. Enfin, le blocage des voies erks par un inhibiteur de mek (sl327) abolit la preference de place conditionnee induite par la cocaine et le thc ainsi que la sensibilisation locomotrice induite par une administration repetee de cocaine sans toutefois affecter les reponses comportementales aigues induites par ces deux drogues. L'activation des erks dans les cellules striatales constituerait un mecanisme commun d'action de ces drogues. En controlant une premiere vague de regulations geniques, cette voie de transduction jouerait un role majeur dans les adaptations neuronales responsables des comportements addictifs a long terme.

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Serotonin 2B receptors in mesoaccumbens dopamine pathway regulate cocaine responses

HAL (Le Centre pour la Communication Scientifique Directe) (2017)

Stéphane Doly Emily Quentin Raphaël Eddine Stefania Tolu Sebastián P. Fernández

Endogenous agonist

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Dopamine signaling in the striatum

Advances in protein chemistry and structural biology (2019)

Emmanuel Valjent Anne Biever Giuseppe Gangarossa Emma Puighermanal

Medium spiny neuron

Biological neural network

10.1016/bs.apcsb.2019.01.004

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Citations (12)

Lack of CB1 cannabinoid receptors modifies nicotine behavioural responses, but not nicotine abstinence

Neuropharmacology (2002)

Anna Castañé Emmanuel Valjent Catherine Ledent Marc Parmentier Rafaël Maldonado

Mecamylamine

Knockout mouse

Conditioned place preference

Rimonabant

Nicotine withdrawal

10.1016/s0028-3908(02)00118-1

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Citations (237)

ERK2: a logical AND gate critical for drug-induced plasticity?

Current Opinion in Pharmacology (2006)

Jean‐Antoine Girault Emmanuel Valjent Jocelyne Caboche Denis Hervé

Conditioned place preference

10.1016/j.coph.2006.08.012

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Citations (338)

Gα_olfMutation Allows Parsing the Role of cAMP-Dependent and Extracellular Signal-Regulated Kinase-Dependent Signaling in l-3,4-Dihydroxyphenylalanine-Induced Dyskinesia

Journal of Neuroscience (2012)

Cristina Alcacer Emanuela Santini Emmanuel Valjent Florence Gaven Jean‐Antoine Girault

Although L-3,4-dihydroxyphenylalanine (L-DOPA) remains the reference treatment of Parkinson's disease, its long-term beneficial effects are hindered by L-DOPA-induced dyskinesia (LID). In the dopamine (DA)-denervated striatum, L-DOPA activates DA D₁ receptor(D₁R) signaling, including cAMP-dependent protein kinase A (PKA) and extracellular signal-regulated kinase (ERK), two responses associated with LID. However, the cause of PKA and ERK activation, their respective contribution to LID, and their relationship are not known. In striatal neurons, D₁R activates adenylyl-cyclase through Gα(olf), a protein upregulated after lesion of DA neurons in rats and inpatients. We report here that increased Gα(olf) levels in hemiparkinsonian mice are correlated with LID after chronic L-DOPA treatment. To determine the role of this upregulation, we performed unilateral lesion in mice lacking one allele of the Gnal gene coding for Gα(olf) (Gnal⁺/⁻). Despite an increase in the lesioned striatum,Gα(olf) levels remained below those of unlesioned wild-type mice. In Gnal⁺/⁻ mice, the lesion-induced L-DOPA stimulation of cAMP/PKA-mediated phosphorylation of GluA1 Ser845 and DARPP-32 (32 kDa DA- and cAMP-regulated phosphoprotein) Thr34 was dramatically reduced, whereas ERK activation was preserved. LID occurrence was similar in Gnal⁺/⁺ and Gnal⁺/⁻ mice after a 10-d L-DOPA (20 mg/kg) treatment. Thus, in lesioned animals, Gα(olf) upregulation is critical for the activation by L-DOPA of D₁R-stimulated cAMP/PKA but not ERK signaling. Although the cAMP/PKA pathway appears to be required for LID development, our results indicate that its activation is unlikely to be the main source of LID. In contrast, the persistence of L-DOPA-induced ERK activation in Gnal⁺/⁻ mice supports its causal role in LID development.

10.1523/jneurosci.0837-12.2012

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Citations (81)

Mitogen-Activated Protein Kinase/Extracellular Signal-Regulated Kinase Induced Gene Regulation in Brain

Molecular Neurobiology (2001)

Jocelyne Caboche Emmanuel Valjent Peter Vanhoutte

ASK1

Cyclin-dependent kinase 5

MAPK cascade

Immediate early gene

10.1385/mn:23:2-3:083

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Citations (107)