Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Loss of Ethanol Inhibition of N-Methyl-D-Aspartate Receptor-Mediated Currents and Plasticity of Cerebellar Synapses in Mice Expressing the GluN1(F639A) Subunit.

Alcoholism, clinical and experimental research - 1 Apr 2018

Zamudio-Bulcock Paula A, Homanics Gregg E, Woodward John J

Abstract excerpt

BACKGROUND: Glutamatergic N-methyl-d-aspartate receptors (NMDARs) are well known for their sensitivity to ethanol (EtOH) inhibition. However, the specific manner in which EtOH inhibits channel activity and how such inhibition affects neurotransmission, and ultimately behavior, remains unclear. Replacement of phenylalanine 639 with alanine (F639A) in the GluN1 subunit reduces EtOH inhibition of recombinant NMDARs....

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cerebellum
Share to Deep Brain Stimulation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Ethanol

Share to Excitatory Postsynaptic Potentials

Share to Neural Inhibition

Share to Neuronal Plasticity

Share to Receptors, N-Methyl-D-Aspartate

Share to Synapses

Source

Open in PubMed Open full text

Identifiers

PMID: 29323417
DOI: 10.1111/acer.13597
PMCID: PMC5880713

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Loss of Ethanol Inhibition of N-Methyl-D-Aspartate Receptor-Mediated Currents and Plasticity of Cerebellar Synapses in Mice Expressing the GluN1(F639A) Subunit.PMID 29323417Read ↗

Prenatal ethanol exposure impairs hippocampal plasticity and cognition in adolescent miceSemantic proximity Read ↗

Ethanol inhibition of N-methyl-D-aspartate receptors is reduced by site-directed mutagenesis of a transmembrane domain phenylalanine residue.Semantic proximity Read ↗

Altered sedative effects of ethanol in mice with α1 glycine receptor subunits that are insensitive to Gβγ modulation.Semantic proximity Read ↗

Importance of genetics in fetal alcohol effects: null mutation of the nNOS gene worsens alcohol-induced cerebellar neuronal losses and behavioral deficits.Semantic proximity Read ↗

Mutation of the inhibitory ethanol site in GABAA ρ1 receptors promotes tolerance to ethanol-induced motor incoordination.Semantic proximity Read ↗

Pharmacologically Counteracting a Phenotypic Difference in Cerebellar GABAA Receptor Response to Alcohol Prevents Excessive Alcohol Consumption in a High Alcohol-Consuming Rodent Genotype.Semantic proximity Read ↗

NR1 knockdown mice as a representative model of the glutamate hypothesis of schizophrenia.Semantic proximity Read ↗

Conditional rescue of protein kinase C epsilon regulates ethanol preference and hypnotic sensitivity in adult mice.Semantic proximity Read ↗

Genetic variation in cerebellar nicotinic acetylcholine receptor (nAChR) function impacts efficacy of nicotine and varenicline treatment of alcohol withdrawal-induced motor impairment.Semantic proximity Read ↗

Alcohol Suppresses Tonic GABAA Receptor Currents in Cerebellar Granule Cells in the Prairie Vole: A Neural Signature of High-Alcohol-Consuming Genotypes.Semantic proximity Read ↗

Transgenic expression of a mutant glycine receptor decreases alcohol sensitivity of mice.Semantic proximity Read ↗

Postnatal NMDA receptor ablation in corticolimbic interneurons confers schizophrenia-like phenotypes.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.