Contribution of Na_v1.8 sodium channels to retinal function

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• 作者：Benjamin J. Smith^a ; ^{BN948751@dal.ca} ; Patrice D. Cô ; té ; ^a ; ^b ; ^&dagger ; ; ^{patrice@dal.ca} ; Franç ; ois Tremblay^b ; ^c ; ^&dagger ; ; ^{ftrembla@dal.ca}
• 关键词：CNS ; central nervous system ; ERG ; electroretinogram ; IT ; implicit time ; Nav ; voltage-gated sodium channel ; OPs ; oscillatory potentials ; PSTHs ; post-stimulus time histograms ; RGCs ; retinal ganglion cells ; rmANOVA ; repeated-measures ANOVA ; SBACs ; starburst amacrine cells
• 刊名：Neuroscience
• 出版年：2017
• 出版时间：6 January 2017
• 年：2017
• 卷：340
• 期：Complete
• 页码：279-290
• 全文大小：2400 K
• 卷排序：340

文摘

Sodium channel isoform Nav1.8 contributions to retinal function were studied using the specific blocker A803467. A803467 had no effect on ERG a- and b-waves, but significantly reduced the oscillatory potentials (OPs). Targeting starburst amacrine cells (SBACs) with the cholinergic neurotoxin AF64A reduced OPs similar to A803467. A803467 affect ON-sustained retinal ganglion cells (RGCs) directly and ON/OFF transient though inhibitory circuits. SBACs, through Nav1.8 modulation, selectively amplify/propagate OPs; Nav1.8 modulates specific aspects of RGC physiology.