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Absence of voltage-dependent calcium channels delays photoreceptor degeneration in rd mice
Daniel S Read1, Maureen A McCall, Ronald G Gregg
1Department of Biochemistry and Molecular Biology, University of Louisville, KY 40202, USA.
Abstract:
Retinal degeneration results from the apoptotic cell death of photoreceptors. While mutations in a large number of genes give rise to retinal degeneration, the specific mechanisms are not well understood. One hypothesis involves mediation of apoptosis by high concentrations of intracellular Ca(2+). We used a mouse line that carries the rd mutation but also lacks the major L-type voltage-dependent Ca(2+) channel at the photoreceptor synapse to examine whether this route of Ca(2+) entry plays a role in photoreceptor degeneration. In both experimental and control mice, the photoreceptors degenerate. However, at postnatal days 16, 18, and 21 there is a delay in photoreceptor cell loss in the experimental mice, which lack L-type voltage-dependent Ca(2+) channels, compared to controls. These data indicate that Ca(2+) entry via the L-type voltage-dependent Ca(2+) channel contributes to the mechanisms responsible for photoreceptor cell death in this mouse model of retinitis pigmentosa.
Insights
Calcium channels contribute to photoreceptor cell death in retinitis pigmentosa. Blocking L-type voltage-dependent calcium channels in mice delayed photoreceptor loss, suggesting a therapeutic target for retinal degeneration.
Area of Science:
- Neuroscience
- Ophthalmology
- Cell Biology
Background:
- Retinal degeneration involves photoreceptor apoptosis.
- Mechanisms of photoreceptor cell death are not fully understood.
- High intracellular calcium (Ca2+) concentrations may mediate apoptosis.
Purpose of the Study:
- To investigate the role of L-type voltage-dependent calcium channels in photoreceptor degeneration.
- To determine if blocking Ca2+ entry affects photoreceptor cell death in a mouse model of retinitis pigmentosa.
Main Methods:
- Utilized a mouse model with the rd mutation lacking L-type voltage-dependent Ca2+ channels at the photoreceptor synapse.
- Compared photoreceptor cell loss in experimental mice (lacking channels) to control mice.
- Assessed cell loss at specific postnatal days (16, 18, 21).
Main Results:
- Photoreceptors degenerated in both experimental and control mice.
- A delay in photoreceptor cell loss was observed in experimental mice lacking L-type voltage-dependent Ca2+ channels.
- This delay was evident at postnatal days 16, 18, and 21.
Conclusions:
- Ca2+ entry through L-type voltage-dependent calcium channels contributes to photoreceptor cell death.
- These channels are implicated in the mechanisms of degeneration in this mouse model of retinitis pigmentosa.
- Targeting these channels may offer a therapeutic strategy for retinal degeneration.
