ArticleNeuron2016
Developmental Inhibition of Gsk3 Rescues Behavioral and Neurophysiological Deficits in a Mouse Model of Schizophrenia Predisposition.
Article in Neuron, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
64 citing papers in PubMed.
- Altered thalamo-prefrontal synchrony dynamics during spatial working memory task performance in a SETD1A loss-of-function mouse model of schizophrenia predisposition.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Divergent transcriptomic pathways underlie sex-biased cognitive rescue by developmental GSK3B inhibition in a mouse model of 22q11.2 deletion syndrome.Translational psychiatry · 2026Article
- Interhemispheric CA1 projections to the subiculum support spatial cognition and are affected in a mouse model of the 22q11.2 deletion syndrome.Cell reports · 2026Article
- Altered thalamo-prefrontal synchrony dynamics during spatial working memory task performance in a SETD1A loss-of-function mouse model of schizophrenia predisposition.bioRxiv : the preprint server for biology · 2026Article
- An ace in the hole? Opportunities and limits of using mice to understand schizophrenia neurobiology.Molecular psychiatry · 2025Review
- Unraveling the enigma of mental disorders: a genetics-first approach and the role of mouse models based on rare disease-susceptible genome variants.Nagoya journal of medical science · 2025Review
- Synaptic-dependent developmental dysconnectivity in 22q11.2 deletion syndrome.Science advances · 2025Article
- Sex-specific maladaptive responses to acute stress upon in utero THC exposure are mediated by dopamine.Pharmacological research · 2024Article
- Synaptic-dependent developmental dysconnectivity in 22q11.2 deletion syndrome.bioRxiv : the preprint server for biology · 2024Article
- Neurobiology of schizophrenia.Current opinion in neurobiology · 2024Review
- Loss of spines in the prelimbic cortex is detrimental to working memory in mice with early-life adversity.Molecular psychiatry · 2023Article
- Using Nonhuman Primate Models to Reverse-Engineer Prefrontal Circuit Failure Underlying Cognitive Deficits in Schizophrenia.Current topics in behavioral neurosciences · 2023Review
- The role of glycogen synthase kinase 3 beta in neurodegenerative diseases.Frontiers in molecular neuroscience · 2023Review
- Prefrontal Interneurons: Populations, Pathways, and Plasticity Supporting Typical and Disordered Cognition in Rodent Models.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Review
- Article
- Review
- Glycogen Synthase Kinase 3: Ion Channels, Plasticity, and Diseases.International journal of molecular sciences · 2022Review
- S-SCAM inhibits Axin-dependent synaptic function of GSK3β in a sex-dependent manner.Scientific reports · 2022Article
- Parvalbumin expressing interneurons control spike-phase coupling of hippocampal cells to theta oscillations.Scientific reports · 2022Article
- Sex Differences in Cognitive Impairment Induced by Cerebral Microhemorrhage.Translational stroke research · 2021Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
While the genetic basis of schizophrenia is increasingly well characterized, novel treatments will require establishing mechanistic relationships between specific risk genes and core phenotypes. Rare, highly penetrant risk genes such as the 22q11.2 microdeletion are promising in this regard. Df(16)A(+/-) mice, which carry a homologous microdeletion, have deficits in hippocampal-prefrontal connectivity that correlate with deficits in spatial working memory. These mice also have deficits in axonal development that are accompanied by dysregulated Gsk3β signaling and can be rescued by Gsk3 antagonists. Here we show that developmental inhibition of Gsk3 rescues deficits in hippocampal-prefrontal connectivity, task-related neural activity, and spatial working memory behavior in Df(16)A(+/-) mice. Taken together, these results provide mechanistic insight into how the microdeletion results in cognitive deficits, and they suggest possible targets for novel therapies.
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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.