Neurexin1 – Nrxn1 Knockout Rat

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Genetically engineered models (GEMS) Neurexin1 – Nrxn1 knockout rat Model Neurexin1 – Nrxn1 knockout rat Strain HsdSage:SD-Nrxn1tm1Sage Location U.S. Availability Cryopreserved Characteristics/husbandry Origin + This model was created in collaboration with Autism The Neurexin1 - Nrxn1 KO rat model was originally created Speaks and has undergone phenotypic characterization at SAGE Labs, Inc. in St. Louis, MO and distributed out of the by Dr. Richard Paylor at Baylor College of Medicine Boyertown, PA facility. The line continues to be maintained through the original SAGE Labs animal inventory acquired Deletions in Neurexin 1 are present in ~0.5% of patients + by Envigo. with ASD + Copy number variations in Neurexin 1 have been linked to both ASD and schizophrenia Description This model contains a biallelic deletion of the Neurexin 1 Neurexins are important for postsynaptic differentiation, + gene (Nrxn1). Mutations in Nrxn1 have been associated with especially so for GABA synaptic connections autism spectrum disorders (ASD) and this model is useful for + Background strain: Sprague Dawley understanding the role of neurexins in the development of ASD. Zygosity genotype + Cryopreserved as heterozygous embryos Research use + Autism + Schizophrenia + Synaptic plasticity North America 800.793.7287 EU and Asia envigo.com/contactus [email protected] envigo.com Figure 1: 16 bp deletion within Exon 1. Neurexin 1 knockout rats possess a 16 bp deletion (red) in Exon 1 (white). The blue region represents the ZFN binding site. Deletion Z inding Site on Figure 2: Age and weight comparison chart HOM male HOM female HET male HET female 00 00 500 00 00 Weight gras Weight 00 100 0 2 4 6 8 10 1 1 1 Age ees Contact us North America 800.793.7287 [email protected] Envigo, 8520 Allison Pointe Blvd., Suite 400, Indianapolis, IN 46250, United States © 2020 Envigo..

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Cellular and Synaptic Network Defects in Autism
Cellular and synaptic network defects in autism The MIT Faculty has made this article openly available. Please share how this access benefits you. Your story matters. Citation Peca, Joao, and Guoping Feng. “Cellular and Synaptic Network Defects in Autism.” Current Opinion in Neurobiology 22, no. 5 (October 2012): 866–872. As Published http://dx.doi.org/10.1016/j.conb.2012.02.015 Publisher Elsevier Version Author's final manuscript Citable link http://hdl.handle.net/1721.1/102179 Terms of Use Creative Commons Attribution-Noncommercial-NoDerivatives Detailed Terms http://creativecommons.org/licenses/by-nc-nd/4.0/ NIH Public Access Author Manuscript Curr Opin Neurobiol. Author manuscript; available in PMC 2013 October 01. Published in final edited form as: Curr Opin Neurobiol. 2012 October ; 22(5): 866–872. doi:10.1016/j.conb.2012.02.015. Cellular and synaptic network defects in autism João Peça1 and Guoping Feng1,2 $watermark-text1McGovern $watermark-text Institute $watermark-text for Brain Research, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA 2Stanley Center for Psychiatric Research, Broad Institute, Cambridge, MA 02142, USA Abstract Many candidate genes are now thought to confer susceptibility to autism spectrum disorder (ASD). Here we review four interrelated complexes, each composed of multiple families of genes that functionally coalesce on common cellular pathways. We illustrate a common thread in the organization of glutamatergic synapses and suggest a link between genes involved in Tuberous Sclerosis Complex, Fragile X syndrome, Angelman syndrome and several synaptic ASD candidate genes. When viewed in this context, progress in deciphering the molecular architecture of cellular protein-protein interactions together with the unraveling of synaptic dysfunction in neural networks may prove pivotal to advancing our understanding of ASDs.
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