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Syngap1 Haploinsufficiency Damages a Postnatal Critical Period of Pyramidal Cell Structural Maturation Linked to Cortical Circuit Assembly
Open accessAbstract
Background Genetic haploinsufficiency of SYNGAP1/Syngap1 commonly occurs in developmental brain disorders, such as intellectual disability, epilepsy, schizophrenia, and autism spectrum disorder. Thus, studying mouse models of Syngap1 haploinsufficiency may uncover pathologic developmental processes common among distinct brain disorders.Methods A Syngap1 haploinsufficiency model was used to explore the relationship between critical period dendritic spine abnormalities, cortical circuit assembly, and the window for genetic rescue to understand how damaging mutations disrupt key substrates of mouse brain development.Results Syngap1 mutations broadly disrupted a developmentally sensitive period that corresponded to the period of heightened postnatal cortical synaptogenesis. Pathogenic Syngap1 mutations caused a coordinated acceleration of dendrite elongation and spine morphogenesis and pruning of these structures in neonatal cortical pyramidal neurons. These mutations also prevented a form of developmental structural plasticity associated with experience-dependent reorganization of brain circuits. Consistent with these findings, Syngap1 mutant mice displayed an altered pattern of long-distance synaptic inputs into a cortical area important for cognition. Interestingly, the ability to genetically improve the behavioral endophenotype of Syngap1 mice decreased slowly over postnatal development and mapped onto the developmental period of coordinated dendritic insults.Conclusions Pathogenic Syngap1 mutations have a profound impact on the dynamics and structural integrity of pyramidal cell postsynaptic structures known to guide the de novo wiring of nascent cortical circuits. These findings support the idea that disrupted critical periods of dendritic growth and spine plasticity may be a common pathologic process in developmental brain disorders.
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“As reported previously,24,29,39 morphological analyses at P21 revealed that dendritic spine head size was significantly smaller in Srgap2 heterozygous CPNs and significantly larger in Syngap1 heterozygous CPNs compared with wild-type layer 2/3 CPNs (Figures 6B–6D and S10D).”
From Synaptic neoteny of human cortical neurons requires species-specific balancing of SRGAP2-SYNGAP1 cross-inhibition (2024) · cites this paper as [39]
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“Previous work has pointed to increased synapse formation in Syngap1+/− juvenile mutant mice, suggestive of accelerated synaptic development.39”
From Synaptic neoteny of human cortical neurons requires species-specific balancing of SRGAP2-SYNGAP1 cross-inhibition (2024) · cites this paper as [39]
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“As reported previously,24,29,39 analysis at P21 revealed that dendritic spine head size was smaller and dendritic spine density higher in SRGAP2C gain-of-function CPNs24,29 (Figures 6B–6D and S10B–S10D).”
From Synaptic neoteny of human cortical neurons requires species-specific balancing of SRGAP2-SYNGAP1 cross-inhibition (2024) · cites this paper as [39]
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“Studies using genetically modified mice that mimic the Syngap1 deficit have revealed precocious dendritic arborization, early formation and premature pruning of dendritic spines as well as enlarged dendritic spines in layer V pyramidal neurons of the somatosensory cortex during a critical period of development, compared to WT mice [2].”
From Autism spectrum disorder: neuropathology and animal models (2017) · cites this paper as [2]
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Citations
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BackgroundInfluentialSelf-citationOne gene, many neuropsychiatric disorders: lessons from Mendelian diseases
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BackgroundSynGAP Regulates Steady-State and Activity-Dependent Phosphorylation of Cofilin
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“The developmental dysregulation of cortical circuits appears to arise from aberrant neonatal synaptogenesis, including precocious and accelerated spine morphogenesis, leading to reduced critical period plasticity and altered long-range circuit connectivity (Aceti et al., 2015).”
BackgroundInfluential
Metadata
- Authors
- Aceti, M., Creson, T. K., Vaissiere, T., Rojas, C., Huang, W.-C., Wang, Y.-X., Petralia, R. S., Page, D. T., Miller, C. A., & Rumbaugh, G.
- Affiliations
- Scripps Research Institute (US)
- National Institutes of Health (US)
- ORCID
- Venue
- Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2015-05
- Volume
- 77
- Issue
- 9
- Pages
- 805-815
- ISSN
- 0006-3223 (ISSN-L)
- PMC
- PMC4326604
- OpenAlex
- W2007942788
- Cited by
- 129
- References
- 44
- Citations by year
- 2026: 11 · 2025: 12 · 2024: 13 · 2023: 14 · 2022: 14 · 2021: 14 · 2020: 12 · 2019: 11 · 2018: 10 · 2017: 11 · 2016: 6 · 2015: 1
- FWCI
- 3.93
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- The National Institute for Neurological Disorders and Stroke (R01NS064079)
- The National Institute for Mental Health (R01MH096847)
- National Institute for Drug Abuse (R01 DA034116, R03 DA033499)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genomic variations and chromosomal abnormalities
- Keywords
- SYNGAP1, haploinsufficiency, dendritic spine maturation, cortical pyramidal neurons, synaptogenesis, dendrite elongation, synaptic pruning, experience-dependent plasticity, intellectual disability, epilepsy, autism spectrum disorder, schizophrenia, genetic rescue, mouse model
- MeSH terms
- Animals, Animals, Newborn, Cerebral Cortex, Conditioning, Psychological, Exploratory Behavior, Fear, Hippocampus, Mice, Transgenic, Neural Pathways, Sensory Deprivation, Vibrissae, Pyramidal Cells, Maze Learning, ras GTPase-Activating Proteins, Dendritic Spines, Haploinsufficiency, Endophenotypes
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