['Retinal ganglion cells expressing the photopigment melanopsin are intrinsically photosensitive (ipRGCs). These ganglion cell photoreceptors send axons to several central targets involved in a variety of functions. Within the retina ipRGCs provide excitatory drive to dopaminergic amacrine cells via glutamatergic signals and ipRGCs are coupled to wide-field GABAergic amacrine cells via gap junctions. However, the extent to which ipRGCs are coupled to other retinal neurons in the ganglion cell layer via gap junctions is unclear. Carbenoxolone, a widely employed gap junction inhibitor, greatly reduces the number of retinal neurons exhibiting non-rod, non-cone mediated light-evoked Ca(2+) signals suggesting extensive intercellular coupling between ipRGCs and non-ipRGCs in the ganglion cell layer. However, carbenoxolone may directly inhibit light-evoked Ca(2+) signals in ipRGCs independent of gap junction blockade.', 'To test the possibility that carbenoxolone directly inhibits light-evoked Ca(2+) responses in ipRGCs, the light-evoked rise in intracellular Ca(2+) ([Ca(2+)](i)) was examined using fura-2 imaging in isolated rat ipRGCs maintained in short-term culture in the absence and presence of carbenoxolone. Carbenoxolone at 50 and 100 µM concentrations completely abolished the light-evoked rise in [Ca(2+)](i) in isolated ipRGCs. Recovery from carbenoxolone inhibition was variable.'] Does carbenoxolone block the light-evoked rise in intracellular calcium in isolated melanopsin ganglion cell photoreceptors?