Vascular Endothelial Growth Factor Modulates Voltage-Gated Na+ Channel Properties and Depresses Action Potential Firing in Cultured Rat Hippocampal Neurons
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- Sun Guang-chun
- Department of Pharmacy, The Fifth People’s Hospital of Shanghai, Fudan University
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- Ma Yuan-yuan
- State Key Laboratory of Medical Neurobiology, Shanghai Medical College, Fudan University
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説明
Vascular endothelial growth factor (VEGF), an angiogenic factor, was found to modulate synaptic plasticity by affecting K+ and Ca2+ channels and protect neuron from death by depressing glutamatergic transmission. However, whether VEGF also modulates neuronal activity through modulating voltage-gated Na+ channels (VGSCs), a main determinant of neuronal excitability, we observed the effects of VEGF on Na+ channel properties and function on cultured rat hippocampal neurons through whole-cell patch-clamp recording. We found that VEGF decreased the Na+ channel excitability by shifting the voltage-dependence of steady-state inactivation to more hyperpolarized direction, and increasing the time constants of recovery from inactivation without significantly affecting the activation process. The effect of VEGF on Na+ channel steady-state inactivation was inhibited by the specific VEGF Flk-1 receptor antagonist SU1498, but was not affected by protein kinase C (PKC)-activator 1-oleoyl-2-acetyl-sn-glycerol (OAG). Furthermore, the inhibition of Na+ currents by VEGF was frequency-dependent. In addition, the frequency of neuron firing evoked by current injection was reversibly depressed by VEGF. Therefore, our results suggest a potential role of VGSCs in the modulation of VEGF on neuronal excitability.
収録刊行物
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- Biological & Pharmaceutical Bulletin
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Biological & Pharmaceutical Bulletin 36 (4), 548-555, 2013
公益社団法人 日本薬学会
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詳細情報 詳細情報について
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- CRID
- 1390282679608935552
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- NII論文ID
- 130003361396
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- NII書誌ID
- AA10885497
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- COI
- 1:STN:280:DC%2BC3szht1CltA%3D%3D
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- ISSN
- 13475215
- 09186158
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- NDL書誌ID
- 024369397
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- PubMed
- 23337128
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- 本文言語コード
- en
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- 資料種別
- journal article
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- データソース種別
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- NDLサーチ
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- PubMed
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