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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Wiley
2017-01-01
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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. |
format | Article |
id | doaj-art-637b51904553492bb3952415782de0f8 |
institution | Kabale University |
issn | 2090-5904 1687-5443 |
language | English |
publishDate | 2017-01-01 |
publisher | Wiley |
record_format | Article |
series | Neural Plasticity |
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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