The lack of CB1 receptors prevents neuroadapatations of both NMDA and GABA(A) receptors after chronic ethanol exposure

Autor: Warnault, Vincent, Houchi, Hakim, Barbier, Estelle, Pierrefiche, Olivier, Vilpoux, Catherine, Ledent, Catherine, Daoust, Martine, Naassila, Mickaël
Přispěvatelé: Groupe de Recherche sur l'alcool et les pharmacodépendances - UMR INSERM_S 1247 (GRAP), Université de Picardie Jules Verne (UPJV)-Institut National de la Santé et de la Recherche Médicale (INSERM), Naassila, Mickael
Jazyk: angličtina
Rok vydání: 2007
Předmět:
Male
MESH: Receptor
Cannabinoid
CB1
MESH: Mice
Knockout
MESH: Dose-Response Relationship
Drug
Mice
Receptor
Cannabinoid
CB1
MESH: Animals
MESH: Brain Chemistry
MESH: Receptors
GABA-A
MESH: Alcohol-Induced Disorders
Nervous System
Mice
Knockout
Muscimol
musculoskeletal
neural
and ocular physiology
Brain
MESH: Excitatory Amino Acid Antagonists
MESH: Protein Subunits
Adaptation
Physiological
Alcoholism
lipids (amino acids
peptides
and proteins)
[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]
psychological phenomena and processes
MESH: Ethanol
MESH: Binding
Competitive
Binding
Competitive
Receptors
N-Methyl-D-Aspartate
MESH: Brain
Alcohol-Induced Disorders
Nervous System
MESH: GABA Agonists
MESH: Alcoholism
Animals
RNA
Messenger
[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]
GABA Agonists
MESH: Mice
MESH: RNA
Messenger
Brain Chemistry
MESH: Receptors
N-Methyl-D-Aspartate
Binding Sites
Dose-Response Relationship
Drug
Ethanol
MESH: Chronic Disease
Receptors
GABA-A
MESH: Adaptation
Physiological
MESH: Male
Disease Models
Animal
Protein Subunits
nervous system
MESH: Binding Sites
Chronic Disease
MESH: Disease Models
Animal
Excitatory Amino Acid Antagonists
MESH: Muscimol
Zdroj: Journal of Neurochemistry
Journal of Neurochemistry, 2007, 102 (3), pp.741-52. ⟨10.1111/j.1471-4159.2007.04577.x⟩
Journal of Neurochemistry, Wiley, 2007, 102 (3), pp.741-52. ⟨10.1111/j.1471-4159.2007.04577.x⟩
ISSN: 0022-3042
1471-4159
DOI: 10.1111/j.1471-4159.2007.04577.x⟩
Popis: International audience; As the contribution of cannabinoid (CB1) receptors in the neuroadaptations following chronic alcohol exposure is unknown, we investigated the neuroadaptations induced by chronic alcohol exposure on both NMDA and GABA(A) receptors in CB1-/- mice. Our results show that basal levels of hippocampal [(3)H]MK-801 ((1)-5-methyl-10,11-dihydro-5Hdibenzo[a,d]cyclohepten-5,10-imine) binding sites were decreased in CB1-/- mice and that these mice were also less sensitive to the locomotor effects of MK-801. Basal level of both hippocampal and cerebellar [(3)H]muscimol binding was lower and sensitivity to the hypothermic effects of diazepam and pentobarbital was increased in CB1-/- mice. GABA(A)alpha1, beta2, and gamma2 and NMDA receptor (NR) 1 and 2B subunit mRNA levels were altered in striatum of CB1-/- mice. Our results also showed that [(3)H]MK-801 binding sites were increased in cerebral cortex and hippocampus after chronic ethanol ingestion only in wild-type mice. Chronic ethanol ingestion did not modify the sensitivity to the locomotor effects of MK-801 in both genotypes. Similarly, chronic ethanol ingestion reduced the number of [(3)H]muscimol binding sites in cerebral cortex, but not in cerebellum, only in CB1+/+ mice. We conclude that lifelong deletion of CB1 receptors impairs neuroadaptations of both NMDA and GABA(A) receptors after chronic ethanol exposure and that the endocannabinoid/CB1 receptor system is involved in alcohol dependence.
Databáze: OpenAIRE
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