Changes in Synaptic Transmission and Long-term Potentiation Induction as a Possible Mechanism for Learning Disability in an Animal Model of Multiple Sclerosis

Changes in Synaptic Transmission and Long-term Potentiation Induction as a Possible Mechanism for Learning Disability in an Animal Model of Multiple Sclerosis


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نویسندگان: محمدرضا پالیزوان , قاسم مسیبی , معصومه مصلح , محمدرضا سلیمان میگونی , مصطفی خلیلی درمنی

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نشریه: International Neurourology Journal, 1,20,26 - 32,2016

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کد مقاله 3326
عنوان فارسی مقاله Changes in Synaptic Transmission and Long-term Potentiation Induction as a Possible Mechanism for Learning Disability in an Animal Model of Multiple Sclerosis
عنوان لاتین مقاله Changes in Synaptic Transmission and Long-term Potentiation Induction as a Possible Mechanism for Learning Disability in an Animal Model of Multiple Sclerosis
نوع مقاله بر حسب نگارش پژوهشی اصیل
مقاله برحسب نمایه ISI
IF 1.061
عنوان نشریه International Neurourology Journal
نوع نشریه علمی پژوهشی
شماره نشریه 1
دوره 20
صفحه شروع و پایان در نشریه 26 - 32
سال انتشار/ ارائه شمسی 1395
سال انتشار/ارائه میلادی 2016
آدرس لینک مقاله/ همایش در شبکه اینترنت http://apps.webofknowledge.com/full_record.do?product=UA&search_mode=GeneralSearch&qid=2&SID=Q2ZyX6qsN9IEa7ND5iy&page=1&doc=1
ISSN 2093-4777
DOI DOI: 10.5213/inj.1632514.257
آدرس علمی (Affiliation) نویسنده متقاضی Department of Microbiology and Immunology, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran

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چکیده انگلیسیChanges in Synaptic Transmission and Long-term Potentiation Induction as a Possible Mechanism for Learning Disability in an Animal Model of Multiple Sclerosis Mosayebi G1, Soleyman MR1, Khalili M1, Mosleh M2, Palizvan MR2.  Department of Microbiology and Immunology, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran.  2Department of Physiology, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran. Abstract PURPOSE: Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system. It has been shown that memory deficits is common in patients with MS. Recent studies using experimental autoimmune encephalomyelitis (EAE) as an animal model of MS have shown that indicated that EAE causes hippocampal-dependent impairment in learning and memory. Thus far, there have been no in vivo electrophysiological reports describing synaptic transmission in EAE animals. The aim of the present work is to evaluate the synaptic changes in the CA1 region of the hippocampus of EAE rats. METHODS: To evaluate changes in synaptic transmission in the CA1 region of the hippocampus of EAE rats, field excitatory postsynaptic potentials (fEPSPs) from the stratum radiatum of CA1 neurons, were recorded following Schaffer collateral stimulation. RESULTS: The results showed that EAE causes deficits in synaptic transmission and long-term potentiation (LTP) in the hippocampus. In addition, paired-pulse index with a 120 msec interstimulus interval was decreased in the EAE group. These findings indicate that EAE might induce suppression in synaptic transmission and LTP by increasing the inhibitory effect of GABAB receptors on the glutamate-mediated EPSP. CONCLUSIONS: In conclusion, influence of inflammation-triggered mechanisms on synaptic transmission may explain the negative effect of EAE on learning abilities in rats. KEYWORDS: Encephalomyelitis, Autoimmune, Experimental; Hippocampus; Long-term Potentiation; Paired Pulse Index
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3326.pdfچکیده لاتین1395/02/13297541دانلود

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نویسنده نفر چندم مقاله
محمدرضا پالیزوانپنجم و مسئول
قاسم مسیبیاول
معصومه مصلحچهارم
محمدرضا سلیمان میگونیدوم
مصطفی خلیلی درمنیسوم

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inj-1632514-257.pdfمتن مقاله1395/01/17345117دانلود