Modulation Effects of Cordycepin on Voltage-Gated Sodium Channels in Rat Hippocampal CA1 Pyramidal Neurons in the Presence/Absence of Oxygen

Our previous study revealed that cordycepin features important neuroprotective effects against hypoxic insult by improvement of neuronal electrophysiological function. Modulation on voltage-gated sodium channel (VGSC) in CA1 neurons is the initial event during hypoxia/ischemia. However, no study com...

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Main Authors: Zhi-Bin Liu, Chao Liu, Bin Zeng, Li-Ping Huang, Li-Hua Yao
Format: Article
Language:English
Published: Wiley 2017-01-01
Series:Neural Plasticity
Online Access:http://dx.doi.org/10.1155/2017/2459053
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author Zhi-Bin Liu
Chao Liu
Bin Zeng
Li-Ping Huang
Li-Hua Yao
author_facet Zhi-Bin Liu
Chao Liu
Bin Zeng
Li-Ping Huang
Li-Hua Yao
author_sort Zhi-Bin Liu
collection DOAJ
description Our previous study revealed that cordycepin features important neuroprotective effects against hypoxic insult by improvement of neuronal electrophysiological function. Modulation on voltage-gated sodium channel (VGSC) in CA1 neurons is the initial event during hypoxia/ischemia. However, no study comprehensively investigated cordycepin on VGSC. Hence, this study investigated modulation effects of cordycepin on VGSC not only in oxygen physiological conditions but also in acute oxygen deprivation injury conditions. Results revealed that cordycepin (80 μM) reduced the amplitude of VGSC currents (INa) (77.6% of control, p<0.01) within 1 min of drug exposure coupled with a negative shift in steady-state inactivation and prolonged recovery time course from inactivation. Additionally, this mild reduction on the peak of INa induced by the pretreatment with cordycepin can attenuate and delay the following hypoxia causing rapid dramatic decrease in INa with no additive change in the voltage dependence of inactivation. As modulation on VGSC in CA1 neurons represents the initial event during ischemia, we propose that suppression effect of cordycepin on VGSC is an important neuronal protective mechanism that may enhance neuronal tolerance to acute oxygen deprivation and delay hypoxia-induced neuronal injuries.
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spelling doaj-art-637b51904553492bb3952415782de0f82025-02-03T01:21:39ZengWileyNeural Plasticity2090-59041687-54432017-01-01201710.1155/2017/24590532459053Modulation Effects of Cordycepin on Voltage-Gated Sodium Channels in Rat Hippocampal CA1 Pyramidal Neurons in the Presence/Absence of OxygenZhi-Bin Liu0Chao Liu1Bin Zeng2Li-Ping Huang3Li-Hua Yao4School of Sport Science, Jiangxi Science & Technology Normal University, Nanchang, Jiangxi 330013, ChinaSchool of Life Science, Jiangxi Science & Technology Normal University, Nanchang, Jiangxi 330013, ChinaSchool of Life Science, Jiangxi Science & Technology Normal University, Nanchang, Jiangxi 330013, ChinaSchool of Pharmacy, Jiangxi University of Traditional Chinese Medicine, Nanchang, Jiangxi 330004, ChinaSchool of Sport Science, Jiangxi Science & Technology Normal University, Nanchang, Jiangxi 330013, ChinaOur previous study revealed that cordycepin features important neuroprotective effects against hypoxic insult by improvement of neuronal electrophysiological function. Modulation on voltage-gated sodium channel (VGSC) in CA1 neurons is the initial event during hypoxia/ischemia. However, no study comprehensively investigated cordycepin on VGSC. Hence, this study investigated modulation effects of cordycepin on VGSC not only in oxygen physiological conditions but also in acute oxygen deprivation injury conditions. Results revealed that cordycepin (80 μM) reduced the amplitude of VGSC currents (INa) (77.6% of control, p<0.01) within 1 min of drug exposure coupled with a negative shift in steady-state inactivation and prolonged recovery time course from inactivation. Additionally, this mild reduction on the peak of INa induced by the pretreatment with cordycepin can attenuate and delay the following hypoxia causing rapid dramatic decrease in INa with no additive change in the voltage dependence of inactivation. As modulation on VGSC in CA1 neurons represents the initial event during ischemia, we propose that suppression effect of cordycepin on VGSC is an important neuronal protective mechanism that may enhance neuronal tolerance to acute oxygen deprivation and delay hypoxia-induced neuronal injuries.http://dx.doi.org/10.1155/2017/2459053
spellingShingle Zhi-Bin Liu
Chao Liu
Bin Zeng
Li-Ping Huang
Li-Hua Yao
Modulation Effects of Cordycepin on Voltage-Gated Sodium Channels in Rat Hippocampal CA1 Pyramidal Neurons in the Presence/Absence of Oxygen
Neural Plasticity
title Modulation Effects of Cordycepin on Voltage-Gated Sodium Channels in Rat Hippocampal CA1 Pyramidal Neurons in the Presence/Absence of Oxygen
title_full Modulation Effects of Cordycepin on Voltage-Gated Sodium Channels in Rat Hippocampal CA1 Pyramidal Neurons in the Presence/Absence of Oxygen
title_fullStr Modulation Effects of Cordycepin on Voltage-Gated Sodium Channels in Rat Hippocampal CA1 Pyramidal Neurons in the Presence/Absence of Oxygen
title_full_unstemmed Modulation Effects of Cordycepin on Voltage-Gated Sodium Channels in Rat Hippocampal CA1 Pyramidal Neurons in the Presence/Absence of Oxygen
title_short Modulation Effects of Cordycepin on Voltage-Gated Sodium Channels in Rat Hippocampal CA1 Pyramidal Neurons in the Presence/Absence of Oxygen
title_sort modulation effects of cordycepin on voltage gated sodium channels in rat hippocampal ca1 pyramidal neurons in the presence absence of oxygen
url http://dx.doi.org/10.1155/2017/2459053
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