Celsr3 is Required for Normal Development of GABA Circuits in the Inner Retina
Author Information
Author(s): Lewis Alaron, Wilson Neil, Stearns George, Johnson Nicolas, Nelson Ralph, Brockerhoff Susan E.
Primary Institution: Department of Biochemistry, University of Washington, Seattle, Washington, United States of America
Hypothesis
The identity of the specific molecules required for the process of retinal circuitry formation is largely unknown.
Conclusion
Celsr3 is critical for normal development of inhibitory circuits within the inner retina, affecting GABA modulation of ON-bipolar cells.
Supporting Evidence
- Celsr3 mRNA is abundant in the amacrine and ganglion cells of the retina.
- The absence of Celsr3 leads to a specific defect in the development of GABAergic signaling.
- Mutant zebrafish exhibit a super-normal b-wave in the electroretinogram (ERG).
- An increase in GABA receptors on mutant ON-bipolar terminals was observed.
- Blastula transplantation experiments indicated that the lack of an OKR is due, at least partially, to Celsr3-mediated defects within the brain.
Takeaway
Celsr3 is a protein that helps the retina work properly, and without it, the signals that help us see can get mixed up.
Methodology
The study involved behavioral assays, electroretinogram (ERG) recordings, and in situ hybridization to analyze the effects of the celsr3 mutation in zebrafish.
Limitations
The study does not rule out the possibility of additional defects within the brain contributing to the lack of an optokinetic response.
Participant Demographics
Zebrafish larvae, specifically the zvm7w65 mutant and wild-type controls.
Statistical Information
P-Value
p<0.001
Statistical Significance
p<0.001
Digital Object Identifier (DOI)
Want to read the original?
Access the complete publication on the publisher's website