Impairment of pupillary responses and optokinetic nystagmus in the mGluR6-deficient mouse.

Retinal bipolar cells receive glutamatergic transmission from photoreceptors and mediate a key process in segregating visual signals into ON-center and OFF-center pathways. The segregation of ON responses involves a G protein-coupled metabotropic glutamate receptor (mGluR). The mGluR6 subtype is expressed restrictedly at the postsynaptic site of retinal ON-bipolar cells. Ablation of mGluR6 in the ON-bipolar cells by gene targeting results in a loss of ON responses but unchanged OFF responses in visual transmission. Thus, mGluR6 is essential for inducing ON responses. The aims of this study are analyses of visual responsiveness and possible visual dysfunction in mGluR6-deficient mice. We report here that mGluR6-deficient mice have unaltered locomotor activity in a daily light-dark cycle and exhibit light-stimulated induction of Fos immunoreactivity in the suprachiasmatic nucleus. These findings indicate that mGluR6-deficient mice are capable or responding to light stimulation. The mGluR6 deficiency, however, markedly reduces the sensitivity of pupillary responses to light stimulus and severely impairs the ability to drive optokinetic nystagmus in response to visual contrasts. This study thus demonstrates that mGluR6 contributes to discrimination of visual contrasts.