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Plasticity of TRPM1 expression and localization in the wild type and degenerating mouse retina
David Križaj1, Wei Huang, Takahisa Furukawa
1Department of Ophthalmology & Visual Sciences, John A. Moran Eye Center, Salt Lake City, UT 84132, United States. david.krizaj@hsc.utah.edu
Abstract:
The light response in retinal ON bipolar cells is associated with disinhibition of current flow through cation channels recently identified as type 1 members of the melastatin transient receptor potential (TRPM) family. We determined the developmental expression of Trpm1 in the wild type C57BL/6, DBA/2J, DBA2J-Gpnmb mouse retinas and in Pde6brd1 retinas characterized by degeneration of rod photoreceptors. Trpm1 mRNA in wild type retinas was low at birth but exhibited progressive increases in abundance up to early adulthood at postnatal day 21 (P21). Retinal Trpm1 mRNA content did not decrease following loss of photoreceptors. At P21, TRPM1-immunopositive perikarya migrated into the outer nuclear layer. The TRPM1 protein was trafficked to discrete postsynaptic puncta in wild type retinas whereas in adult Pde6brd1 mouse retinas, TRPM1 translocated to bipolar perikarya and bar-like structures in the distal inner nuclear layer. These findings show that expression and localization of the TRPM1 in the mouse retina is plastic, modulated by use-dependence and availability of sustained excitatory input.
Insights
The TRPM1 channel in mouse retinas shows dynamic expression and localization changes during development and in response to photoreceptor degeneration. Its presence is linked to light responses in retinal ON bipolar cells.
Area of Science:
- Neuroscience
- Ophthalmology
- Molecular Biology
Background:
- The light response in retinal ON bipolar cells involves disinhibition of cation channels, specifically TRPM1 (transient receptor potential melastatin 1).
- Understanding TRPM1's developmental and functional role is crucial for retinal circuitry research.
Purpose of the Study:
- To investigate the developmental expression and localization of Trpm1 in mouse retinas.
- To examine Trpm1's plasticity in response to photoreceptor degeneration.
Main Methods:
- Quantitative analysis of Trpm1 mRNA in different mouse retinal models (wild type and Pde6brd1).
- Immunohistochemistry to detect TRPM1 protein localization at various developmental stages and in disease models.
- Comparison of Trpm1 expression and localization in wild-type and photoreceptor-deficient retinas.
Main Results:
- Trpm1 mRNA levels increase progressively from birth to adulthood in wild-type retinas.
- Trpm1 mRNA abundance remains stable even after photoreceptor loss.
- TRPM1 protein exhibits dynamic trafficking, moving to postsynaptic puncta in wild-type and to bipolar cells/inner nuclear layer in degenerated retinas.
Conclusions:
- Retinal TRPM1 expression and localization are plastic, influenced by developmental stage and visual experience.
- TRPM1's adaptability suggests a key role in modulating retinal light responses under varying physiological conditions.
