Figure 5. High-threshold light-evoked synaptic responses survive interruption of primary and secondary rod pathways by Cx36 knockout.

A: Raster plots of light responses in a representative ipRGC from a Cx36 KO mouse recorded first with synapses functional (left) and then with synapses blocked (right). In synaptic blockade, the light response exhibited the long latency and prominent poststimulus persistence of spiking characteristic of melanopsin-mediated responses. With synaptic input intact (left), responses were brisker and more sensitive than the melanopsin-driven response. Because both primary and secondary rod ON pathways were disrupted by the genetic deletion of Cx36, these brisk, synaptically mediated responses were presumably driven by cones. Note that stimulus intensities are not matched in the left and right columns of panel A. Also, stimulus duration was increased 10-fold under synaptic blockade (right) because a 1 sec stimulus was too short to evoke an intrinsic photoresponse at most intensities tested. B: Group irradiance-response data of the sort illustrated in panel A for ten ipRGCs recorded from the same piece of Cx36 KO mouse retina. The triangles along the abscissa indicate the response thresholds (5% of maximum; open triangle, synapses functional; filled triangle, synapses blocked). The presumptive cone-driven response is at least 2 log units more sensitive than the melanopsin drive; the difference would have been greater if stimulus duration had not been increased under synaptic blockade to enhance the intrinsic response. Qualitatively similar results were obtained in a total of 8 retinas (data not shown).