ReviewMolecular psychiatry2014
What causes aberrant salience in schizophrenia? A role for impaired short-term habituation and the GRIA1 (GluA1) AMPA receptor subunit.
Review in Molecular psychiatry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 100 citations in OpenAlex.
- Impaired contingency judgement in mice under ketamine: an implication for an altered sense of agency in schizophrenia.Psychopharmacology · 2026Article
- Genetic and functional insights into long noncoding RNAs in schizophrenia.Molecular psychiatry · 2026Article
- Hippocampal transcriptome profiling in a 22q11.2 deletion syndrome mouse model: comparison with human schizophrenia.Molecular brain · 2026Article
- Comprehensive Assessment of Druggable Targets in Cortical Neurons Reveals Biological Limits of Cell Type-Specific Neuropharmacology.Biomedicines · 2026Article
- The GluA1 cytoplasmic tail regulates intracellular AMPA receptor trafficking and synaptic transmission onto dentate gyrus GABAergic interneurons, gating response to novelty.Molecular psychiatry · 2026Article
- Olfactory-Guided Behavior Uncovers Imaging and Molecular Signatures of Alzheimer's Disease Risk.Brain sciences · 2025Article
- Smelling the Risk: Early Olfactory Deficits, Brain Networks, and Blood Markers of Alzheimer's Disease Risk in Humanized APOE Mice.bioRxiv : the preprint server for biology · 2025Article
- Acute optogenetic induction of the prodromal endophenotype of CA1 hyperactivity causes schizophrenia-related deficits in cognition and salience attribution.Schizophrenia (Heidelberg, Germany) · 2024Article
- Population genetic admixture and evolutionary history in the Shandong Peninsula inferred from integrative modern and ancient genomic resources.BMC genomics · 2024Article
- The antipsychotic agent sulpiride microinjected into the ventral pallidum restores positive symptom-like habituation disturbance in MAM-E17 schizophrenia model rats.Scientific reports · 2024Article
- Novel α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptor (AMPAR) potentiator LT-102: A promising therapeutic agent for treating cognitive impairment associated with schizophrenia.CNS neuroscience & therapeutics · 2024Article
- Article
- GRIN2A (NR2A): a gene contributing to glutamatergic involvement in schizophrenia.Molecular psychiatry · 2023Review
- Glutamatergic dysfunction leads to a hyper-dopaminergic phenotype through deficits in short-term habituation: a mechanism for aberrant salience.Molecular psychiatry · 2023Article
- PGC-1α regulates critical period onset/closure, mediating cortical plasticity.Frontiers in molecular neuroscience · 2023Article
- Article
- Cerebellar glutamatergic system impacts spontaneous motor recovery by regulating Gria1 expression.NPJ Regenerative medicine · 2022Article
- Deep learning predicts DNA methylation regulatory variants in the human brain and elucidates the genetics of psychiatric disorders.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- GSK-3β Disrupts Neuronal Oscillatory Function to Inhibit Learning and Memory in Male Rats.Cellular and molecular neurobiology · 2022Article
- Zika virus-induced TNF-α signaling dysregulates expression of neurologic genes associated with psychiatric disorders.Journal of neuroinflammation · 2022Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The GRIA1 locus, encoding the GluA1 (also known as GluRA or GluR1) AMPA glutamate receptor subunit, shows genome-wide association to schizophrenia. As well as extending the evidence that glutamatergic abnormalities have a key role in the disorder, this finding draws attention to the behavioural phenotype of Gria1 knockout mice. These mice show deficits in short-term habituation. Importantly, under some conditions the attention being paid to a recently presented neutral stimulus can actually increase rather than decrease (sensitization). We propose that this mouse phenotype represents a cause of aberrant salience and, in turn, that aberrant salience (and the resulting positive symptoms) in schizophrenia may arise, at least in part, from a glutamatergic genetic predisposition and a deficit in short-term habituation. This proposal links an established risk gene with a psychological process central to psychosis and is supported by findings of comparable deficits in short-term habituation in mice lacking the NMDAR receptor subunit Grin2a (which also shows association to schizophrenia). As aberrant salience is primarily a dopaminergic phenomenon, the model supports the view that the dopaminergic abnormalities can be downstream of a glutamatergic aetiology. Finally, we suggest that, as illustrated here, the real value of genetically modified mice is not as 'models of schizophrenia' but as experimental tools that can link genomic discoveries with psychological processes and help elucidate the underlying neural mechanisms.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.