ArticlePsychopharmacology2016
A mouse model of the 15q13.3 microdeletion syndrome shows prefrontal neurophysiological dysfunctions and attentional impairment.
Article in Psychopharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Developmentally dynamic, non-convergent transcriptomic profiles in CNV models for schizophrenia risk.Molecular psychiatry · 2026Article
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- Scn1a haploinsufficiency in the prefrontal cortex leads to cognitive impairment and depressive phenotype.Brain : a journal of neurology · 2024Article
- Dissection of neuronal circuits underlying sustained attention with the five-choice serial reaction time task.Neuroscience and biobehavioral reviews · 2023Review
- Mouse Behavior on the Trial-Unique Nonmatching-to-Location (TUNL) Touchscreen Task Reflects a Mixture of Distinct Working Memory Codes and Response Biases.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Impaired OTUD7A-dependent Ankyrin regulation mediates neuronal dysfunction in mouse and human models of the 15q13.3 microdeletion syndrome.Molecular psychiatry · 2023Article
- Use of an Automated Mouse Touchscreen Platform for Quantification of Cognitive Deficits After Central Nervous System Injury.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Altered gene expression profiles impair the nervous system development in individuals with 15q13.3 microdeletion.Scientific reports · 2022Article
- The schizophrenia risk gene Map2k7 regulates responding in a novel contingency-shifting rodent touchscreen gambling task.Disease models & mechanisms · 2022Article
- Computational identification of variables in neonatal vocalizations predictive for postpubertal social behaviors in a mouse model of 16p11.2 deletion.Molecular psychiatry · 2021Article
- Using touchscreen-delivered cognitive assessments to address the principles of the 3Rs in behavioral sciences.Lab animal · 2021Review
- Transcriptomic networks implicate neuronal energetic abnormalities in three mouse models harboring autism and schizophrenia-associated mutations.Molecular psychiatry · 2021Article
- Behavioral Tasks Evaluating Schizophrenia-like Symptoms in Animal Models: A Recent Update.Current neuropharmacology · 2021Review
- Dissociable contributions of mediodorsal and anterior thalamic nuclei in visual attentional performance: A comparison using nicotinic and muscarinic cholinergic receptor antagonists.Journal of psychopharmacology (Oxford, England) · 2020Article
- Clinical and experimental insight into pathophysiology, comorbidity and therapy of absence seizures.Brain : a journal of neurology · 2020Review
- The abiding relevance of mouse models of rare mutations to psychiatric neuroscience and therapeutics.Schizophrenia research · 2020Article
- Interactive effects between hemizygous 15q13.3 microdeletion and peripubertal stress on adult behavioral functions.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019Article
- A Touchscreen Motivation Assessment Evaluated in Huntington's Disease Patients and R6/1 Model Mice.Frontiers in neurology · 2019Article
- Selective effects of 5-HT2C receptor modulation on performance of a novel valence-probe visual discrimination task and probabilistic reversal learning in mice.Psychopharmacology · 2018Article
- Bidirectional Regulation of Aggression in Mice by Hippocampal Alpha-7 Nicotinic Acetylcholine Receptors.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018Article
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Authors and funding
17 authors.
Funding
Abstract
rationaleA microdeletion at locus 15q13.3 is associated with high incidence rates of psychopathology, including schizophrenia. A mouse model of the 15q13.3 microdeletion syndrome has been generated (Df[h15q13]/+) with translational utility for modelling schizophrenia-like pathology. Among other deficits, schizophrenia is characterised by dysfunctions in prefrontal cortical (PFC) inhibitory circuitry and attention.
objectivesThe objective of this study is to assess PFC-dependent functioning in the Df(h15q13)/+ mouse using electrophysiological, pharmacological, and behavioural assays.
methodExperiments 1-2 investigated baseline firing and auditory-evoked responses of PFC interneurons and pyramidal neurons. Experiment 3 measured pyramidal firing in response to intra-PFC GABAA receptor antagonism. Experiments 4-6 assessed PFC-dependent attentional functioning through the touchscreen 5-choice serial reaction time task (5-CSRTT). Experiments 7-12 assessed reversal learning, paired-associate learning, extinction learning, progressive ratio, trial-unique non-match to sample, and object recognition.
resultsIn experiments 1-3, the Df(h15q13)/+ mouse showed reduced baseline firing rate of fast-spiking interneurons and in the ability of the GABAA receptor antagonist gabazine to increase the firing rate of pyramidal neurons. In assays of auditory-evoked responses, PFC interneurons in the Df(h15q13)/+ mouse had reduced detection amplitudes and increased detection latencies, while pyramidal neurons showed increased detection latencies. In experiments 4-6, the Df(h15q13)/+ mouse showed a stimulus duration-dependent decrease in percent accuracy in the 5-CSRTT. The impairment was insensitive to treatment with the partial α7nAChR agonist EVP-6124. The Df(h15q13)/+ mouse showed no cognitive impairments in experiments 7-12.
conclusionThe Df(h15q13)/+ mouse has multiple dysfunctions converging on disrupted PFC processing as measured by several independent assays of inhibitory transmission and attentional function.
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