Deficiency of Dgcr8 , a gene disrupted by the 22q11.2 microdeletion, results in altered short-term plasticity in the prefrontal cortex
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Individuals with 22q11.2 microdeletions have cognitive and behavioral impairments and the highest known genetic risk for developing schizophrenia. One gene disrupted by the 22q11.2 microdeletion is DGCR8 , a component of the “microprocessor” complex that is essential for microRNA production, resulting in abnormal processing of specific brain miRNAs and working memory deficits. Here, we determine the effect of Dgcr8 deficiency on the structure and function of cortical circuits by assessing their laminar organization, as well as the neuronal morphology, and intrinsic and synaptic properties of layer 5 pyramidal neurons in the prefrontal cortex of Dgcr8 +/− mutant mice. We found that heterozygous Dgcr8 mutant mice have slightly fewer cortical layer 2/4 neurons and that the basal dendrites of layer 5 pyramidal neurons have slightly smaller spines. In addition to the modest structural changes, field potential and whole-cell electrophysiological recordings performed in layer 5 of the prefrontal cortex revealed greater short-term synaptic depression during brief stimulation trains applied at 50 Hz to superficial cortical layers. This finding was accompanied by a decrease in the initial phase of synaptic potentiation. Our results identify altered short-term plasticity as a neural substrate underlying the cognitive dysfunction and the increased risk for schizophrenia associated with the 22q11.2 microdeletions.
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Dgcr8+/− mice have fewer layer II and III cortical neurons and reduced spine width, but not spine length, on basal dendrites in prefrontal cortical neurons.
“Some examples include fewer layer II and III cortical neurons and reduced spine width, but not spine length, on basal dendrites in prefrontal cortical neurons of Dgcr8+/− mice [111]”
From Autism spectrum disorder: neuropathology and animal models (2017) · cites this paper as [111]
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- Authors
- Fénelon, K., Mukai, J., Xu, B., Hsu, P.-K., Drew, L. J., Karayiorgou, M., Fischbach, G. D., MacDermott, A. B., & Gogos, J. A.
- Affiliations
- Columbia University Irving Medical Center (US)
- Columbia University (US)
- New York State Psychiatric Institute (US)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2011-02-28
- Volume
- 108
- Issue
- 11
- Pages
- 4447-4452
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC3060227
- OpenAlex
- W2042021963
- Cited by
- 202
- References
- 43
- Citations by year
- 2026: 4 · 2025: 14 · 2024: 8 · 2023: 7 · 2022: 13 · 2021: 7 · 2020: 7 · 2019: 15 · 2018: 8 · 2017: 16 · 2016: 12 · 2015: 18 · 2014: 19 · 2013: 19 · 2012: 21
- FWCI
- 9.67
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- McKnight Endowment Fund for Neuroscience
- March of Dimes Foundation
- McKnight Foundation
- National Alliance for Research on Schizophrenia and Depression
- National Institute of Mental Health (R01MH067068, R01MH077235, MH 67068, MH077235)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genomic variations and chromosomal abnormalities
- Keywords
- DGCR8, 22q11.2 deletion syndrome, microprocessor complex, microRNA processing, short-term plasticity, prefrontal cortex, layer 5 pyramidal neurons, cortical laminar organization, dendritic spines, synaptic depression, synaptic potentiation, schizophrenia risk, working memory deficits
- MeSH terms
- Animals, Chromosome Deletion, Chromosomes, Human, Pair 22, Neuronal Plasticity, Proteins, Synapses, Time Factors, RNA-Binding Proteins, Gene Deletion, Prefrontal Cortex, Excitatory Postsynaptic Potentials, Dendritic Spines, Mice, CA1 Region, Hippocampal, CA3 Region, Hippocampal
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