ArticleFrontiers in cellular neuroscience2016
Overexpression of Isoforms of Nitric Oxide Synthase 1 Adaptor Protein, Encoded by a Risk Gene for Schizophrenia, Alters Actin Dynamics and Synaptic Function.
Article in Frontiers in cellular neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 30 citations in OpenAlex.
- Recessive variants in the intergenic NOS1AP-C1orf226 locus cause monogenic kidney disease responsive to anti-proteinuric treatment.Nature communications · 2025Article
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- Decreased CNNM2 expression in prefrontal cortex affects sensorimotor gating function, cognition, dendritic spine morphogenesis and risk of schizophrenia.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Article
- Blood-Borne Microparticles Are an Inflammatory Stimulus in Type 2 Diabetes Mellitus.ImmunoHorizons · 2023Article
- Circulating endothelial precursor cells are associated with a healed diabetic foot ulcer evaluated in a prospective cohort study.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society · 2023Article
- Förster resonance energy transfer efficiency of the vinculin tension sensor in cultured primary cortical neuronal growth cones.Neurophotonics · 2022Article
- RecessiveScience advances · 2021Article
- Cytosolic PSD-95 interactor alters functional organization of neural circuits and AMPA receptor signaling independent of PSD-95 binding.Network neuroscience (Cambridge, Mass.) · 2021Article
- Diagnosis of traumatic brain injury using miRNA signatures in nanomagnetically isolated brain-derived extracellular vesicles.Lab on a chip · 2018Article
- A Novel Short Isoform of Cytosolic PSD-95 Interactor (Cypin) Regulates Neuronal Development.Molecular neurobiology · 2018Article
- d-Serine administration affects nitric oxide synthase 1 adaptor protein and DISC1 expression in sex-specific manner.Molecular and cellular neurosciences · 2018Article
- Overexpression of cypin alters dendrite morphology, single neuron activity, and network properties via distinct mechanisms.Journal of neural engineering · 2018Article
- Psychiatric behaviors associated with cytoskeletal defects in radial neuronal migration.Cellular and molecular life sciences : CMLS · 2017Review
- Developmental Alcohol Exposure Impairs Activity-Dependent S-Nitrosylation of NDEL1 for Neuronal Maturation.Cerebral cortex (New York, N.Y. : 1991) · 2017Article
- Role of Akt-independent mTORC1 and GSK3β signaling in sublethal NMDA-induced injury and the recovery of neuronal electrophysiology and survival.Scientific reports · 2017Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Proper communication between neurons depends upon appropriate patterning of dendrites and correct distribution and structure of spines. Schizophrenia is a neuropsychiatric disorder characterized by alterations in dendrite branching and spine density. Nitric oxide synthase 1 adaptor protein (NOS1AP), a risk gene for schizophrenia, encodes proteins that are upregulated in the dorsolateral prefrontal cortex (DLPFC) of individuals with schizophrenia. To elucidate the effects of NOS1AP overexpression observed in individuals with schizophrenia, we investigated changes in actin dynamics and spine development when a long (NOS1AP-L) or short (NOS1AP-S) isoform of NOS1AP is overexpressed. Increased NOS1AP-L protein promotes the formation of immature spines when overexpressed in rat cortical neurons from day in vitro (DIV) 14 to DIV 17 and reduces the amplitude of miniature excitatory postsynaptic currents (mEPSCs). In contrast, increased NOS1AP-S protein increases the rate of actin polymerization and the number of immature and mature spines, which may be attributed to a decrease in total Rac1 expression and a reduction in the levels of active cofilin. The increase in the number of mature spines by overexpression of NOS1AP-S is accompanied by an increase in the frequency of mEPSCs. Our findings show that overexpression of NOS1AP-L or NOS1AP-S alters the actin cytoskeleton and synaptic function. However, the mechanisms by which these isoforms induce these changes are distinct. These results are important for understanding how increased expression of NOS1AP isoforms can influence spine development and synaptic function.
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