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Suppressive Effects of Resveratrol Treatment on The Intrinsic Evoked Excitability of CA1 Pyramidal Neurons

OBJECTIVE: Resveratrol, a phytoalexin, has a wide range of desirable biological actions. Despite a growing body of evidence indicating that resveratrol induces changes in neu- ronal function, little effort, if any, has been made to investigate the cellular effect of res- veratrol treatment on intrin...

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Autores principales: Meftahi, Gholamhossein, Ghotbedin, Zohreh, Eslamizade, Mohammad Javad, Hosseinmardi, Narges, Janahmadi, Mahyar
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Royan Institute 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4601874/
https://www.ncbi.nlm.nih.gov/pubmed/26464825
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author Meftahi, Gholamhossein
Ghotbedin, Zohreh
Eslamizade, Mohammad Javad
Hosseinmardi, Narges
Janahmadi, Mahyar
author_facet Meftahi, Gholamhossein
Ghotbedin, Zohreh
Eslamizade, Mohammad Javad
Hosseinmardi, Narges
Janahmadi, Mahyar
author_sort Meftahi, Gholamhossein
collection PubMed
description OBJECTIVE: Resveratrol, a phytoalexin, has a wide range of desirable biological actions. Despite a growing body of evidence indicating that resveratrol induces changes in neu- ronal function, little effort, if any, has been made to investigate the cellular effect of res- veratrol treatment on intrinsic neuronal properties. MATERIALS AND METHODS: This experimental study was performed to examine the acute effects of resveratrol (100 µM) on the intrinsic evoked responses of rat Cornu Ammonis (CA1) pyramidal neurons in brain slices, using whole cell patch clamp re- cording under current clamp conditions. RESULTS: Findings showed that resveratrol treatment caused dramatic changes in evoked responses of pyramidal neurons. Its treatment induced a significant (P<0.05) increase in the after hyperpolarization amplitude of the first evoked action potential. Resveratrol-treated cells displayed a significantly broader action potential (AP) when compared with either control or vehicle-treated groups. In addition, the mean instantaneous firing frequency between the first two action potentials was significantly lower in resveratrol-treated neurons. It also caused a significant reduction in the time to maximum decay of AP. The rheobase current and the utilization time were both significantly greater following resveratrol treatment. Neurons exhibited a significantly depolarized voltage threshold when exposed to resveratrol. CONCLUSION: Results provide direct electrophysiological evidence for the inhibitory effects of resveratrol on pyramidal neurons, at least in part, by reducing the evoked neural activity.
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spelling pubmed-46018742015-10-13 Suppressive Effects of Resveratrol Treatment on The Intrinsic Evoked Excitability of CA1 Pyramidal Neurons Meftahi, Gholamhossein Ghotbedin, Zohreh Eslamizade, Mohammad Javad Hosseinmardi, Narges Janahmadi, Mahyar Cell J Original Article OBJECTIVE: Resveratrol, a phytoalexin, has a wide range of desirable biological actions. Despite a growing body of evidence indicating that resveratrol induces changes in neu- ronal function, little effort, if any, has been made to investigate the cellular effect of res- veratrol treatment on intrinsic neuronal properties. MATERIALS AND METHODS: This experimental study was performed to examine the acute effects of resveratrol (100 µM) on the intrinsic evoked responses of rat Cornu Ammonis (CA1) pyramidal neurons in brain slices, using whole cell patch clamp re- cording under current clamp conditions. RESULTS: Findings showed that resveratrol treatment caused dramatic changes in evoked responses of pyramidal neurons. Its treatment induced a significant (P<0.05) increase in the after hyperpolarization amplitude of the first evoked action potential. Resveratrol-treated cells displayed a significantly broader action potential (AP) when compared with either control or vehicle-treated groups. In addition, the mean instantaneous firing frequency between the first two action potentials was significantly lower in resveratrol-treated neurons. It also caused a significant reduction in the time to maximum decay of AP. The rheobase current and the utilization time were both significantly greater following resveratrol treatment. Neurons exhibited a significantly depolarized voltage threshold when exposed to resveratrol. CONCLUSION: Results provide direct electrophysiological evidence for the inhibitory effects of resveratrol on pyramidal neurons, at least in part, by reducing the evoked neural activity. Royan Institute 2015 2015-10-07 /pmc/articles/PMC4601874/ /pubmed/26464825 Text en Any use, distribution, reproduction or abstract of this publication in any medium, with the exception of commercial purposes, is permitted provided the original work is properly cited http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Meftahi, Gholamhossein
Ghotbedin, Zohreh
Eslamizade, Mohammad Javad
Hosseinmardi, Narges
Janahmadi, Mahyar
Suppressive Effects of Resveratrol Treatment on The Intrinsic Evoked Excitability of CA1 Pyramidal Neurons
title Suppressive Effects of Resveratrol Treatment on The Intrinsic Evoked Excitability of CA1 Pyramidal Neurons
title_full Suppressive Effects of Resveratrol Treatment on The Intrinsic Evoked Excitability of CA1 Pyramidal Neurons
title_fullStr Suppressive Effects of Resveratrol Treatment on The Intrinsic Evoked Excitability of CA1 Pyramidal Neurons
title_full_unstemmed Suppressive Effects of Resveratrol Treatment on The Intrinsic Evoked Excitability of CA1 Pyramidal Neurons
title_short Suppressive Effects of Resveratrol Treatment on The Intrinsic Evoked Excitability of CA1 Pyramidal Neurons
title_sort suppressive effects of resveratrol treatment on the intrinsic evoked excitability of ca1 pyramidal neurons
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4601874/
https://www.ncbi.nlm.nih.gov/pubmed/26464825
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