IMPAIRMENT OF PUPILLARY RESPONSES AND OPTOKINETIC NYSTAGMUS IN THE MGLUR6-DEFICIENT MOUSE

Retinal bipolar cells receive glutamatergic transmission from photorec eptors and mediate a key process in segregating visual signals into ON -center and OFF-center pathways. The segregation of ON responses invol ves a G protein-coupled metabotropic glutamate receptor (mGluR). The m GluR6 subtype is expressed restrictedly at the postsynaptic site of re tinal ON-bipolar cells. Ablation of mGluR6 in the ON-bipolar cells by gene targeting results in a loss of ON responses but unchanged OFF res ponses in visual transmission. Thus, mGluR6 is essential for inducing ON responses. The aims of this study are analyses of visual responsive ness and possible visual dysfunction in mGluR6-deficient mice. We repo rt here that mGluR6-deficient mice have unaltered locomotor activity i n a daily light-dark cycle and exhibit light-stimulated induction of F os immunoreactivity in the suprachiasmatic nucleus. These findings ind icate that mGluR6-deficient mice are capable of responding to light st imulation. The mGluR6 deficiency, however, markedly reduces the sensit ivity of pupillary responses to light stimulus and severely impairs th e ability to drive optokinetic nystagmus ill response to visual contra sts. This study thus demonstrates that mGluR6 contributes to discrimin ation of visual contrasts. (C) 1997 Elsevier Science Ltd.