ArticleTranslational psychiatry2019
Downregulation of Npas4 in parvalbumin interneurons and cognitive deficits after neonatal NMDA receptor blockade: relevance for schizophrenia.
Article in Translational psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Prefrontal and Hippocampal Parvalbumin Interneurons in Animal Models for Schizophrenia: A Systematic Review and Meta-analysis.Schizophrenia bulletin · 2024Pooled it
- Disruption of psychostimulant-associated memories by single, low dose ketamine in rats.Neuropharmacology · 2026Article
- Npas4 is involved in synaptic and cognitive function by regulating the transcription of Neuroligin-1 and N-cadherin.Translational psychiatry · 2026Article
- Transcription Factors in the Pathogenesis of Schizophrenia.Life (Basel, Switzerland) · 2026Review
- Memory-Associated Immediate Early Genes: Roles in Synaptic Function, Memory Processes, and Neurological Diseases.Molecular neurobiology · 2025Review
- Fast-spiking parvalbumin-positive interneurons: new perspectives of treatment and future challenges in dementia.Molecular psychiatry · 2025Review
- Sensory Stimulation-dependent Npas4 Expression in the Olfactory Bulb during Early Postnatal Development.Experimental neurobiology · 2024Article
- Origin and functional diversification of PAS domain, a ubiquitous intracellular sensor.Science advances · 2023Article
- Cortical interneurons in schizophrenia - cause or effect?Croatian medical journal · 2023Review
- Identification of a GABAergic neural circuit governing leptin signaling deficiency-induced obesity.eLife · 2023Article
- Article
- Elevation of EGR1/zif268, a Neural Activity Marker, in the Auditory Cortex of Patients with Schizophrenia and its Animal Model.Neurochemical research · 2022Article
- Prepubescent female rodents have enhanced hippocampal LTP and learning relative to males, reversing in adulthood as inhibition increases.Nature neuroscience · 2022Article
- The Participation of the Intrinsically Disordered Regions of the bHLH-PAS Transcription Factors in Disease Development.International journal of molecular sciences · 2021Article
- The Engram's Dark Horse: How Interneurons Regulate State-Dependent Memory Processing and Plasticity.Frontiers in neural circuits · 2021Review
- [Advances on GABAergic interneurons in autism spectrum disorders].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2020Review
- Chronic treatment with the antipsychotic drug blonanserin modulates the responsiveness to acute stress with anatomical selectivity.Psychopharmacology · 2020Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysfunction of prefrontal parvalbumin (PV+) interneurons has been linked with severe cognitive deficits as observed in several neurodevelopmental disorders including schizophrenia. However, whether a specific aspect of PV+ neurons deregulation, or a specific molecular mechanism within PV+ neurons is responsible for cognitive deficits and other behavioral impairments remain to be determined. Here, we induced cognitive deficits and altered the prefrontal PV system in mice by exposing them neonatally to the NMDA receptor antagonist ketamine. We observed that the cognitive deficits and hyperactivity induced by neonatal ketamine were associated with a downregulation of Npas4 expression specifically in PV+ neurons. To determine whether Npas4 downregulation-induced dysfunction of PV+ neurons could be a molecular contributor to the cognitive and behavioral impairments reported after neonatal ketamine, we used a transgenic Cre-Lox approach. Reduced Npas4 expression within PV+ neurons replicates deficits in short-term memory observed after neonatal ketamine, but does not reproduce disturbances in general activity. Our data show for the first time that the brain-specific transcription factor Npas4 may be an important contributor to PV+ neurons dysfunction in neurodevelopmental disorders, and thereby could contribute to the cognitive deficits observed in diseases characterized by abnormal functioning of PV+ neurons such as schizophrenia. These findings provide a potential novel therapeutic target to rescue the cognitive impairments of schizophrenia that remain to date unresponsive to treatments.
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