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

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 indicate...

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Main Authors: Ghasem Mosayebi, Mohammad Reza Soleyman, Mostafa khalili, Masoumeh Mosleh, Mohammad Reza Palizvan
Format: Article
Language:English
Published: Korean Continence Society 2016-03-01
Series:International Neurourology Journal
Subjects:
Online Access:http://www.einj.org/upload/pdf/inj-1632514-257.pdf
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author Ghasem Mosayebi
Mohammad Reza Soleyman
Mostafa khalili
Masoumeh Mosleh
Mohammad Reza Palizvan
author_facet Ghasem Mosayebi
Mohammad Reza Soleyman
Mostafa khalili
Masoumeh Mosleh
Mohammad Reza Palizvan
author_sort Ghasem Mosayebi
collection DOAJ
description 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.
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spelling doaj.art-84d170c797db4a0a84f5fbd31e3c86d32022-12-22T00:55:00ZengKorean Continence SocietyInternational Neurourology Journal2093-47772093-69312016-03-01201263210.5213/inj.1632514.257573Changes in Synaptic Transmission and Long-term Potentiation Induction as a Possible Mechanism for Learning Disability in an Animal Model of Multiple SclerosisGhasem Mosayebi0Mohammad Reza Soleyman1Mostafa khalili2Masoumeh Mosleh3Mohammad Reza Palizvan4 Department of Microbiology and Immunology, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran Department of Microbiology and Immunology, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran Department of Microbiology and Immunology, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran Department of Physiology, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran Department of Physiology, Faculty of Medicine, Arak University of Medical Sciences, Arak, IranPurpose: 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.http://www.einj.org/upload/pdf/inj-1632514-257.pdfEncephalomyelitis, Autoimmune, ExperimentalHippocampusLong-term PotentiationPaired Pulse Index
spellingShingle Ghasem Mosayebi
Mohammad Reza Soleyman
Mostafa khalili
Masoumeh Mosleh
Mohammad Reza Palizvan
Changes in Synaptic Transmission and Long-term Potentiation Induction as a Possible Mechanism for Learning Disability in an Animal Model of Multiple Sclerosis
International Neurourology Journal
Encephalomyelitis, Autoimmune, Experimental
Hippocampus
Long-term Potentiation
Paired Pulse Index
title Changes in Synaptic Transmission and Long-term Potentiation Induction as a Possible Mechanism for Learning Disability in an Animal Model of Multiple Sclerosis
title_full Changes in Synaptic Transmission and Long-term Potentiation Induction as a Possible Mechanism for Learning Disability in an Animal Model of Multiple Sclerosis
title_fullStr Changes in Synaptic Transmission and Long-term Potentiation Induction as a Possible Mechanism for Learning Disability in an Animal Model of Multiple Sclerosis
title_full_unstemmed Changes in Synaptic Transmission and Long-term Potentiation Induction as a Possible Mechanism for Learning Disability in an Animal Model of Multiple Sclerosis
title_short Changes in Synaptic Transmission and Long-term Potentiation Induction as a Possible Mechanism for Learning Disability in an Animal Model of Multiple Sclerosis
title_sort changes in synaptic transmission and long term potentiation induction as a possible mechanism for learning disability in an animal model of multiple sclerosis
topic Encephalomyelitis, Autoimmune, Experimental
Hippocampus
Long-term Potentiation
Paired Pulse Index
url http://www.einj.org/upload/pdf/inj-1632514-257.pdf
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