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Updated: Mar 10, 2026

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Immunohistochemical and Calcium Imaging Methods in Wholemount Rat Retina
Published on: October 13, 2014
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Contribution of Nav1.8 sodium channels to retinal function
Benjamin J Smith1, Patrice D Côté2, François Tremblay3
1Department of Biology, Dalhousie University, 1355 Oxford St., PO Box 15000, Halifax, NS B3H 4R2, Canada.
Neuroscience
|December 17, 2016
Summary
The sodium channel Nav1.8 significantly impacts retinal function by reducing oscillatory potentials (OPs), suggesting starburst amacrine cells (SBACs) are key contributors to this electroretinogram component.
Area of Science:
- Neuroscience
- Ophthalmology
- Electrophysiology
Background:
- The sodium channel isoform Nav1.8 is expressed in specific retinal neurons.
- Its precise role in retinal function, particularly in electroretinogram (ERG) components beyond the b-wave, remains unclear.
Purpose of the Study:
- To investigate the contribution of Nav1.8 to retinal function using a specific blocker.
- To elucidate the cellular mechanisms underlying Nav1.8's effects on retinal signaling and ERG components.
Main Methods:
- Utilized the specific Nav1.8 blocker A803467 to assess its impact on ERG.
- Recorded light responses from retinal ganglion cells (RGCs) using a multielectrode array (MEA).
- Investigated the role of starburst amacrine cells (SBACs) by targeting them with ethylcholine mustard aziridinium (AF64A).
Main Results:
- A803467 significantly reduced ERG oscillatory potentials (OPs) amplitude by 40-60% with altered implicit times.
- Nav1.8 blockade caused opposing effects on ON-sustained (decrease) and ON-OFF transient (increase) RGCs.
- Targeting SBACs with AF64A mimicked the OP reduction observed with A803467.
Conclusions:
- Nav1.8 plays a crucial role in modulating specific aspects of retinal physiology, particularly OPs.
- Starburst amacrine cells (SBACs) are identified as a fundamental cellular contributor to mouse retinal OPs.
- Highlights a functional dichotomy between ERG b-waves and OPs in the mouse retina.
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