In darkness, glutamate released from photoreceptors activates the mGluR6 receptor on retinal ON bipolar cells, and this activates the G-protein Go, leading to a closure of TRPM1 channel and cells hyperpolarization.It has been generally assumed that deleting mGluR6 would render the cascade inactive and ON bipolar cells constitutively depolarized.Surprisingly, in mGluR6-null mice, we found that the rod bipolar cells were constitutively hyperpolarized.The slope conductance of the Ⅰ-Ⅴ curves and the current noise were smaller than in wild type.Furthermore, while in wild type it was possible to activate TRPM1 by local application of the TRPV1 agonist capsaicin (in 6/15 cells), in null rod bipolar cells such attempts failed (32 cells).These results suggest that the TRPM1 channel in mGluR6 null rod bipolar cells is inactive.To explore the reason for this lack of activity, we tested whether deleting mGluR6 affects the expression of the cascade components.