Frontiers in cellular neuroscience, 2019-03, Vol.13, p.111-111
2019
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- Autor(en) / Beteiligte
- Titel
- Altered Behaviors and Impaired Synaptic Function in a Novel Rat Model With a Complete Shank3 Deletion
- Ist Teil von
- Frontiers in cellular neuroscience, 2019-03, Vol.13, p.111-111
- Ort / Verlag
- Switzerland: Frontiers Research Foundation
- Erscheinungsjahr
- 2019
- Quelle
- EZB Electronic Journals Library
- Beschreibungen/Notizen
- Mutations within the gene, which encodes a key postsynaptic density (PSD) protein at glutamatergic synapses, contribute to the genetic etiology of defined autism spectrum disorders (ASDs), including Phelan-McDermid syndrome (PMS) and intellectual disabilities (ID). Although there are a series of genetic mouse models to study gene in ASDs, there are few rat models with species-specific advantages. In this study, we established and characterized a novel rat model with a deletion spanning exons 11-21 of , leading to a complete loss of the major SHANK3 isoforms. Synaptic function and plasticity of -deficient rats were impaired detected by biochemical and electrophysiological analyses. -depleted rats showed impaired social memory but not impaired social interaction behaviors. In addition, impaired learning and memory, increased anxiety-like behavior, increased mechanical pain threshold and decreased thermal sensation were observed in -deficient rats. It is worth to note that -deficient rats had nearly normal levels of the endogenous social neurohormones oxytocin (OXT) and arginine-vasopressin (AVP). This new rat model will help to further investigate the etiology and assess potential therapeutic target and strategy for -related neurodevelopmental disorders.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1662-5102eISSN: 1662-5102DOI: 10.3389/fncel.2019.00111Titel-ID: cdi_doaj_primary_oai_doaj_org_article_651d98408f8040608bce28430ad2c663
- Format
- –
- Schlagworte
- Animal models, Anxiety, Arginine, Argipressin, Autism, autism spectrum disorders, Behavior, Brain research, CRISPR, Etiology, Exons, Gene deletion, Gene mutations, Genetic aspects, Glutamatergic transmission, Intellectual disabilities, Isoforms, Laboratories, Mechanical properties, Memory, Mutation, Neurobiology, Neurodevelopmental disorders, Neuroplasticity, Neuroscience, Neurosciences, Neurotransmitters, Oxytocin, Pain, pain threshold, Pervasive developmental disorders, Phelan-McDermid syndrome, Postsynaptic density, Proteins, Rodents, Shank3, Social interaction, social memory, Synaptic plasticity, Therapeutic applications, Vasopressin