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Acid-sensing ion channel 3 in retinal function and survival
Mohammed Ettaiche1, Emmanuel Deval, Sophie Pagnotta
1Institut de Pharmacologie Moléculaire et Cellulaire, Centre National de la Recherche Scientifique, Université de Nice-Sophia Antipolis, Valbonne, France.
Investigative Ophthalmology & Visual Science
|January 2, 2009
Summary
Acid-sensing ion channel 3 (ASIC3) plays a dual role in retinal health. While its absence initially enhances visual function, it leads to late-onset photoreceptor degeneration and vision loss in aged mice.
Area of Science:
- Neuroscience
- Ophthalmology
- Molecular Biology
Background:
- Extracellular pH changes in the retina impact visual function.
- Acid-sensing ion channel 3 (ASIC3) is a key sensor of acidosis.
- The role of ASIC3 in retinal physiology and pathology is not fully understood.
Purpose of the Study:
- To investigate the expression and function of ASIC3 in the rodent retina.
- To determine the role of ASIC3 in retinal activity, phototransduction, and survival using ASIC3 knockout mice.
Main Methods:
- Immunolocalization of ASIC3 in retinal cells.
- Electroretinography to assess retinal function in wild-type and knockout mice.
- Retinal histology, glial fibrillary acidic protein (GFAP) expression, apoptosis assays (TUNEL), and patch-clamp recordings were performed.
Main Results:
- ASIC3 is expressed in photoreceptors, horizontal cells, amacrine cells, and retinal ganglion cells (RGCs).
- ASIC3 knockout mice show enhanced visual function at 2-3 months but severe retinal degeneration, reduced visual function, and increased apoptosis at 8 months.
- Upregulation of GFAP indicates Müller cell activation in older knockout mice.
Conclusions:
- ASIC3 inactivation initially improves visual transduction but leads to late-onset rod photoreceptor death.
- ASIC3 is crucial for maintaining retinal integrity and preventing age-related retinal degeneration.
