Ethanol-mediated facilitation of AMPA receptor function in the dorsomedial striatum: implications for alcohol drinking behavior.: Ethanol and AMPA receptors in the dorsomedial striatum

Autor: Wang, Jun, Ben Hamida, Sami, Darcq, Emmanuel, Zhu, Wenheng, Gibb, Stuart, Lanfranco, Maria Fe, Carnicella, Sebastien, Ron, Dorit
Přispěvatelé: Savasta, Marc, Cell Biology of Addiction in Neurology, Ernest Gallo Clinic and Research Center, Department of Neurology, University of California [San Francisco] (UC San Francisco), University of California (UC)-University of California (UC), ANTE-INSERM U836, équipe 10, Dynamique des réseaux neuronaux du mouvement, Ernest Gallo Clinic and Research Center-Ernest Gallo Clinic and Research Center-Department of Neurology, University of California (UC)-University of California (UC)-University of California [San Francisco] (UC San Francisco), This research was supported by funds provided by the State of California for medical research on alcohol and substance abuse through the University of California, San Francisco (D.R.), by NIAAA (R01AA/MH13438) (D.R.) and (P50AA017072) (D.R. and J.W.), and by ABMRF/The Foundation for Alcohol Research (J.W.).
Jazyk: angličtina
Rok vydání: 2012
Předmět:
MESH: Sulpiride
MESH: Ethanol
MESH: Rats
[SDV.MHEP.PHY] Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]
MESH: Picrotoxin
MESH: Neurons
MESH: Conditioning
Operant

MESH: Rats
Sprague-Dawley

MESH: GABA Antagonists
MESH: Choice Behavior
MESH: Animals
Newborn

MESH: Corpus Striatum
MESH: Long-Term Potentiation
MESH: Quinoxalines
MESH: Rats
Long-Evans

MESH: Analysis of Variance
MESH: Patch-Clamp Techniques
MESH: Up-Regulation
[SDV.MHEP.PHY]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]
MESH: Animals
[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]
MESH: Excitatory Postsynaptic Potentials
MESH: Food Preferences
MESH: Sweetening Agents
MESH: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid
musculoskeletal
neural
and ocular physiology

fungi
MESH: Sucrose
MESH: Electric Stimulation
MESH: Excitatory Amino Acid Antagonists
MESH: Male
MESH: N-Methylaspartate
MESH: Evoked Potentials
nervous system
MESH: Receptors
AMPA

MESH: Synaptosomes
[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]
MESH: Central Nervous System Depressants
MESH: Excitatory Amino Acid Agonists
MESH: Self Administration
MESH: Dopamine Antagonists
Zdroj: Journal of Neuroscience
Journal of Neuroscience, 2012, 32 (43), pp.15124-32. ⟨10.1523/JNEUROSCI.2783-12.2012⟩
ISSN: 0270-6474
1529-2401
DOI: 10.1523/JNEUROSCI.2783-12.2012⟩
Popis: International audience; We found previously that acute ex vivo as well as repeated cycles of in vivo ethanol exposure and withdrawal, including excessive voluntary consumption of ethanol, produces a long-lasting increase in the activity of NR2B-containing NMDA receptors (NR2B-NMDARs) in the dorsomedial striatum (DMS) of rats (Wang et al., 2010a). Activation of NMDARs is required for the induction of long-term potentiation (LTP) of AMPA receptor (AMPAR)-mediated synaptic response. We therefore examined whether the ethanol-mediated upregulation of NMDAR activity alters the induction of LTP in the DMS. We found that ex vivo acute exposure of striatal slices to, and withdrawal from, ethanol facilitates the induction of LTP in DMS neurons, which is abolished by the inhibition of NR2B-NMDARs. We also report that repeated systemic administration of ethanol causes an NR2B-NMDAR-dependent facilitation of LTP in the DMS. LTP is mediated by the insertion of AMPAR subunits into the synaptic membrane, and we found that repeated systemic administration of ethanol, as well as cycles of excessive ethanol consumption and withdrawal, produced a long-lasting increase in synaptic localization of the GluR1 and GluR2 subunits of AMPARs in the DMS. Importantly, we report that inhibition of AMPARs in the DMS attenuates operant self-administration of ethanol, but not of sucrose. Together, our data suggest that aberrant synaptic plasticity in the DMS induced by repeated cycles of ethanol exposure and withdrawal contributes to the molecular mechanisms underlying the development and/or maintenance of excessive ethanol consumption.
Databáze: OpenAIRE