کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8684611 | 1580132 | 2018 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Impaired social behaviors and minimized oxytocin signaling of the adult mice deficient in the N-methyl-d-aspartate receptor GluN3A subunit
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کلمات کلیدی
5-HTRNMDARNR3AAVPCD73CD38N-methyl-d-aspartate5-HTTNMDATNFR1BDNF - BDNF یا فاکتور نورونزایی مشتقشده از مغز autism spectrum disorders - اختلالات طیف اوتیسمCNS - دستگاه عصبی مرکزیSocial behaviors - رفتارهای اجتماعیserotonin transporter - سروتونین حمل کنندهcentral nervous system - سیستم عصبی مرکزیBrain-derived neurotrophic factor - فاکتور نوروتروفی مشتق شده از مغزknockout - ناکاوتASD - نقص سپتوم یا دیوارهی دهلیزیwild-type - نوع وحشیvasopressin - وازوپرسینN-methyl-d-aspartate receptor - گیرنده N-methyl-d-aspartateSerotonin receptor - گیرنده سروتونینtumor necrosis factor receptor 1 - گیرنده فاکتور نکروز تومور 1
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
عصب شناسی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Impaired social behaviors and minimized oxytocin signaling of the adult mice deficient in the N-methyl-d-aspartate receptor GluN3A subunit Impaired social behaviors and minimized oxytocin signaling of the adult mice deficient in the N-methyl-d-aspartate receptor GluN3A subunit](/preview/png/8684611.png)
چکیده انگلیسی
The N-methyl-d-aspartate receptor (NMDAR) has been implicated in the pathophysiology of neurological diseases, such as schizophrenia, autism spectrum disorders (ASD), and Alzheimer's disease (AD), whose unique clinical hallmark is a constellation of impaired social and/or cognitive behaviors. GluN3A (NR3A) is a unique inhibitory subunit in the NMDAR complex. The role of GluN3A in social behavioral activities is obscure. In this study, we sought to evaluate altered social activities in adult GluN3A knockout (KO) mice. GluN3A KO mice spent less time in reciprocal social interaction in the social interaction test compared to wild-type (WT) mice. A social approach test using a three-chamber system confirmed that mice lacking GluN3A had lower sociability and did not exhibit a preference for social novelty. GluN3A KO mice displayed abnormal food preference in the social transmission of food preference task and low social interaction activity in the five-trial social memory test, but without social memory deficits. Using a home cage monitoring system, we observed reduced social grooming behavior in GluN3A KO mice. Signaling genes that might mediate the altered social behaviors were examined in the prefrontal cortex, hippocampus, and thalamus. Among nine genes examined, the expression of the oxytocin receptor was significantly lower in the prefrontal cortex of GluN3A KO mice than that in WT mice. Oxytocin treatment rescued social activity deficits in GluN3A KO mice. These findings support a novel idea that a chronic state of moderate increases in NMDAR activities may lead to downregulation of the oxytocin signaling and impaired behavioral activities that are seen in psychiatric/neurodegenerative disorders.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Neurology - Volume 305, July 2018, Pages 1-12
Journal: Experimental Neurology - Volume 305, July 2018, Pages 1-12
نویسندگان
Jin Hwan Lee, James Ya Zhang, Zheng Zachory Wei, Shan Ping Yu,