ArticleMolecular psychiatry2024
Frontostriatal circuit dysfunction leads to cognitive inflexibility in neuroligin-3 R451C knockin mice.
Article in Molecular psychiatry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 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
5 citing papers in PubMed, 6 citations in OpenAlex.
- Cholecystokinin upregulation in mPFC leads to social defeat-induced anxiety susceptibility in neuroligin 3 R451C knockin mice.Molecular autism · 2026Article
- Cadherin 11 regulates presynaptic vesicle trafficking and neuronal activity in autism-related brain circuit.Molecular psychiatry · 2026Article
- A simple method that doubles learning speed for mice in touchscreen-based visual discrimination.Scientific reports · 2025Article
- Training Schedule Affects Operant Responding Independent of Motivation in the Neuroligin-3 R451C Mouse Model of Autism.Genes, brain, and behavior · 2025Article
- tDCS-induced enhancement of cognitive flexibility in autism: role of frontal lobe and associated neural circuits.Frontiers in behavioral neuroscience · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 6 institutions in 2 countries.
Funding
Abstract
Cognitive and behavioral rigidity are observed in various psychiatric diseases, including in autism spectrum disorder (ASD). However, the underlying mechanism remains to be elucidated. In this study, we found that neuroligin-3 (NL3) R451C knockin mouse model of autism (KI mice) exhibited deficits in behavioral flexibility in choice selection tasks. Single-unit recording of medium spiny neuron (MSN) activity in the nucleus accumbens (NAc) revealed altered encoding of decision-related cue and impaired updating of choice anticipation in KI mice. Additionally, fiber photometry demonstrated significant disruption in dynamic mesolimbic dopamine (DA) signaling for reward prediction errors (RPEs), along with reduced activity in medial prefrontal cortex (mPFC) neurons projecting to the NAc in KI mice. Interestingly, NL3 re-expression in the mPFC, but not in the NAc, rescued the deficit of flexible behaviors and simultaneously restored NAc-MSN encoding, DA dynamics, and mPFC-NAc output in KI mice. Taken together, this study reveals the frontostriatal circuit dysfunction underlying cognitive inflexibility and establishes a critical role of the mPFC NL3 deficiency in this deficit in KI mice. Therefore, these findings provide new insights into the mechanisms of cognitive and behavioral inflexibility and potential intervention strategies.
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Registered trials
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.