Vertebrate vision: TRP channels in the spotlight

Abstract

The recent discovery of the critical role of TRPM1 in retinal function in vertebrates has come as a surprise and has already provided important insights into a common cause of blindness

Figure 1

Segregation of ON and OFF channels at the photoreceptor-bipolar cell synapse. Glutamate, which is released by photoreceptor terminals in the dark, opens AMPA/KA receptor channels on OFF bipolar cells (left) and activates mGluR6 on ON bipolar cells (right). Because mGluR6 is negatively coupled to a cation-selective transduction channel, binding of glutamate to mGluR6 keeps the cation channel closed and the ON bipolar cells in a hyperpolarized state. The decrease in glutamate release in response to light triggers the closure of the AMPA/KA receptor channel and hyperpolarization of OFF bipolar cells and the opening of the mGluR6-gated cation channel and the depolarization of ON bipolar cells (see [2] for details). Despite intensive research, the molecular nature of the mGluR6-gated channel has remained elusive. Recent evidence indicates that transient receptor potential M1 (TRPM1) is the mGluR6-gated channel.