کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6827604 | 548157 | 2011 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Medial prefrontal cortical synapsin II knock-down induces behavioral abnormalities in the rat: Examining synapsin II in the pathophysiology of schizophrenia
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کلمات کلیدی
Synapsin IIVMAT2PFCAPDVAMPPPISNAP-25VGLUT2aCSFVGLUT1VGATMPFCSchizophrenia - اسکیزوفرنی یا شیزوفرنیsodium dodecyl sulfate-polyacrylamide gel electrophoresis - الکتروفورز ژل دوده سولفات سدیم پلی آکریل آمیدSDS-PAGE - الکتروفورز ژل پلی آکریل آمیدanalysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of variancevesicular GABA transporter - حامل ویسکوزر GABAvesicular glutamate transporter 2 - حمل کننده گلوتامات vesicular 2vesicular glutamate transporter 1 - حمل کننده گلوتامات وزیکولار 1Intraperitoneally - داخل صفاقیAntipsychotic drug - دارو ضدپرسیAntipsychotic drugs - داروهای ضد روانپریشیdecibel - دسیبلDopamine - دوپامینcentimeter - سانتیمترprefrontal cortex - قشر prefrontalmedial prefrontal cortex - قشر غده پروسترولartificial cerebral spinal fluid - مایع مغزی نخاعی مغزیPrepulse inhibition - مهار پیش قاعدگیvesicular monoamine transporter 2 - مونوآمین حامل 2Vesicle-associated membrane protein - پروتئین غشاء مرتبط با Vesiclesynaptosomal-associated protein 25 - پروتئین مرتبط با سیناپتوزوموم 25GABA - گاباglutamate - گلوتامات
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب رفتاری
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Synapsin II is a synaptic vesicle-associated phosphoprotein that has been implicated in the pathophysiology of schizophrenia. Studies have demonstrated reductions in synapsin II mRNA and protein in medial prefrontal cortical post-mortem samples from patients with schizophrenia, genetic associations between synapsin II and schizophrenia, and synapsin II protein regulation by dopamine receptor activation. Collectively, this research indicates a relationship between synapsin II dysregulation and schizophrenia; however, it remains unknown whether perturbations in synapsin II play a role in the pathophysiology of this disease. The aim of this project was to evaluate animals with selective knock-down of synapsin II in the medial prefrontal cortex. After continuous infusion of synapsin II antisense sequences, animals were examined for the presence of schizophrenic-like behavioral phenotypes and assessed on the response to clinically relevant antipsychotic drugs. Our results indicate that rats with selective reductions in medial prefrontal cortical synapsin II demonstrate deficits in sensorimotor gating (prepulse inhibition), reduced social behavior, and hyperlocomotion, which are corrected by the atypical antipsychotic drug olanzapine. Additionally, synapsin II knock-down disrupts serial search efficiency. These behavioral changes are accompanied by reductions in vesicular neurotransmitter transporter protein concentrations for glutamate (VGLUT1 and VGLUT2) and GABA (VGAT), without affecting dopamine (VMAT2). These results implicate a causal role for decreased synapsin II in the medial prefrontal cortex in the pathophysiology of schizophrenia and the mechanisms of aberrant prefrontal cortical circuitry, and suggest that synapsin II may potentially serve as a novel therapeutic target for this disorder.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Schizophrenia Research - Volume 130, Issues 1â3, August 2011, Pages 250-259
Journal: Schizophrenia Research - Volume 130, Issues 1â3, August 2011, Pages 250-259
نویسندگان
Bailey A. Dyck, Michael G.R. Beyaert, Mark A. Ferro, Ram K. Mishra,