Cited by 203Neuroscience and Neuropharmacology ResearchSchizophrenia research and treatmentGenomic variations and chromosomal abnormalities

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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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Fénelon, Karine, Mukai, Jun, Xu, Bin, Hsu, Pei-Ken, Drew, Liam J., Karayiorgou, Maria, Fischbach, Gerald D., MacDermott, Amy B., Gogos, Joseph A.·2011·Proceedings of the National Academy of Sciences

DOI 10.1073/pnas.1101219108PMC PMC3060227

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Abstract

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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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)
ORCID: Fénelon, Karine
Mukai, Jun
Xu, Bin
Karayiorgou, Maria
Gogos, Joseph A.
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
DOI: 10.1073/pnas.1101219108
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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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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