Voltage-gated calcium channels are abnormal in cultured spinal motoneurons in the G93A-SOD1 transgenic mouse model of ALS
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- 作者：Qing Changa ; qchang1@jhmi.edu" class="auth_mail" title="E-mail the corresponding author ; Lee J. Martina ; b
- 关键词：ALS ; amyotrophic lateral sclerosis ; SOD1 ; superoxide dismutase-1 ; AMPA ; α-amino-3-hydroxy-5-methylisoxazole propionic acid ; VGCC ; voltage-gated Ca2 ; + channel ; PCCa ; persistent Ca2 ; + current ; mSOD1 ; mutant SOD1 ; TEA-Cl ; tetraethylammonium chloride ; 4-AP ; 4-aminopyridine ; TTX ; tetrodotoxin ; AP ; action potential ; PSC ; postsynaptic current ; sEPSC ; spontaneous excitatory postsynaptic current ; sIPSC ; spontaneous inhibitory postsynaptic current ; mEPSC ; miniature excitatory postsynaptic curren
- 刊名：Neurobiology of Disease
- 出版年：2016
- 出版时间：September 2016
- 年：2016
- 卷：93
- 期：Complete
- 页码：78-95
- 全文大小：3554 K
文摘
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We examined voltage-gated Ca2 + channels in cultured motoneurons in G93A-SOD1 mice.
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G93A-SOD1 motoneurons exhibit increased high voltage activated Ca2 + currents.
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G93A-SOD1 motoneurons also display altered persistent Ca2 + currents.
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G93A-SOD1 motoneurons have altered Ca2 + channel mRNA expression and immunoreactivity.
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Voltage-gated Ca2 + channels might contribute to ALS pathogenesis.