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Related Experiment Video

Updated: May 19, 2026

Yeast Luminometric and Xenopus Oocyte Electrophysiological Examinations of the Molecular Mechanosensitivity of TRPV4

Yeast Luminometric and Xenopus Oocyte Electrophysiological Examinations of the Molecular Mechanosensitivity of TRPV4

Published on: December 31, 2013

Depolarizing bipolar cell dysfunction due to a Trpm1 point mutation.

Neal S Peachey¹, Jillian N Pearring, Pasano Bojang

¹Louis Stokes Cleveland Department of Veterans Affairs Medical Center, Cleveland, Ohio 44106, USA. neal.peachey@va.gov

Journal of Neurophysiology

|August 17, 2012

Summary

This summary is machine-generated.

A new mouse model, Trpm1(tvrm27), reveals a dominant-negative TRPM1 mutation causing impaired vision. This finding advances understanding of congenital stationary night blindness and TRPM1 channel function in the retina.

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Area of Science:

Genetics
Neuroscience
Ophthalmology

Background:

Mutations in TRPM1 cause a form of congenital stationary night blindness (cCSNB).
The Trpm1 knockout mouse (Trpm1(-/-)) is a model for cCSNB.
A novel mouse mutant, tvrm27, was identified.

Purpose of the Study:

To characterize the genetic mutation and phenotype of the tvrm27 mouse.
To investigate the functional consequences of the mutation on TRPM1 channel activity.
To explore the role of TRPM1 in retinal signal transduction and visual processing.

Main Methods:

Genetic mapping to identify the mutation locus.
Complementation testing with Trpm1(-/-) mice.
DNA sequencing to pinpoint the specific nucleotide change.
Electroretinography (ERG) to assess retinal function.
Electrophysiological recordings (whole-cell) of retinal cells.

Main Results:

The tvrm27 mutation was mapped to the Trpm1 gene, resulting in a p.A1068T substitution in the TRPM1 pore domain.
Trpm1(tvrm27/tvrm27) mice showed retained TRPM1 expression at depolarizing bipolar cell (DBC) dendritic tips, unlike Trpm1(-/-) mice.
Heterozygous Trpm1(+/tvrm27) mice exhibited reduced ERG b-wave amplitudes and impaired DBC responses, indicating a dominant-negative effect.
The study identified the number of functional TRPM1 channels at DBC dendritic tips as crucial for DBC response amplitude.

Conclusions:

The p.A1068T mutation in TRPM1 acts in a dominant-negative manner, impairing TRPM1 channel function.
The tvrm27 mouse model is valuable for studying TRPM1's role in DBC signal transduction and central visual processing.
This mutant mouse can aid in evaluating potential therapies for cCSNB.