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

Glutamatergic dysfunction leads to a hyper-dopaminergic phenotype through deficits in short-term habituation: a mechanism for aberrant salience.

Molecular psychiatry - 1 Feb 2023

Panayi Marios C, Boerner Thomas, Jahans-Price Thomas, Huber Anna, Sprengel Rolf, Gilmour Gary, Sanderson David J, Harrison Paul J, Walton Mark E, Bannerman David M

Abstract excerpt

Psychosis in disorders like schizophrenia is commonly associated with aberrant salience and elevated striatal dopamine. However, the underlying cause(s) of this hyper-dopaminergic state remain elusive. Various lines of evidence point to glutamatergic dysfunction and impairments in synaptic plasticity in the etiology of schizophrenia, including deficits associated with the GluA1 AMPAR subunit. GluA1 knockout...

Read the complete abstract on PubMed

Topics

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

Share to Dopamine
Share to Habituation, Psychophysiologic

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Memory, Short-Term

Share to Mice, Knockout

Share to Phenotype

Source

Open in PubMed Open full text

Identifiers

PMID: 36460723
DOI: 10.1038/s41380-022-01861-8
PMCID: PMC9908551

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Glutamatergic dysfunction leads to a hyper-dopaminergic phenotype through deficits in short-term habituation: a mechanism for aberrant salience.PMID 36460723Read ↗

GRIN2A (NR2A): a gene contributing to glutamatergic involvement in schizophrenia.Semantic proximity Read ↗

Behavioral and neurochemical phenotyping of Homer1 mutant mice: possible relevance to schizophrenia.Semantic proximity Read ↗

Behavioral phenotyping and dopamine dynamics in mice with conditional deletion of the glutamate transporter GLT-1 in neurons: resistance to the acute locomotor effects of amphetamine.Semantic proximity Read ↗

Targeting Amygdala-Brainstem Synapses to Reverse Prepulse Inhibition DeficitsSemantic proximity Read ↗

Grin2a knockout in adolescent dopamine neurons disrupts prediction error signaling and produces a phenotype relevant to schizophrenia.Semantic proximity Read ↗

GlyT-1 Inhibition Attenuates Attentional But Not Learning or Motivational Deficits of the Sp4 Hypomorphic Mouse Model Relevant to Psychiatric Disorders.Semantic proximity Read ↗

Prefrontal glutamate correlates of methamphetamine sensitization and preference.Semantic proximity Read ↗

Disrupted activity in the hippocampal-accumbens circuit of type III neuregulin 1 mutant mice.Semantic proximity Read ↗

Assessment of glutamate transporter GLAST (EAAT1)-deficient mice for phenotypes relevant to the negative and executive/cognitive symptoms of schizophrenia.Semantic proximity Read ↗

Neuregulin 1 transgenic mice display reduced mismatch negativity, contextual fear conditioning and social interactions.Semantic proximity Read ↗

Optogenetic interrogation of the role of striatal patches in habit formation and inhibition of striatal dopamineSemantic proximity Read ↗

Decreased dopamine D4 receptor expression increases extracellular glutamate and alters its regulation in mouse striatum.Semantic proximity Read ↗

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