cGMP was proposed to be the agent which directly opens the light-sensitive channel in Limulus ventral photoreceptors. However, the light-sensitive rhabdomeral-lobe (R-lobe) is not uniformly responsive to cGMP injection; that is, there are ‘hot spots’ of sensitivity. A potent phosphodiesterase which rapidly hydrolyses cGMP was suggested to explain the existence of these ‘hot spots’. To test this idea we injected ventral photoreceptors with hydrolysis-resistant cyclic nucleotide analogues. Whereas there can be a lack of a response to cGMP injection into the R-lobe, we find a reproducible depolarization upon R-lobe injection of hydrolysis-resistant cGMP analogues. Furthermore, the depolarization resulting from the injection of cGMP analogues does not require a rise in intracellular Ca2+, as it is not blocked by the Ca2+ buffer, BAPTA. Surprisingly, R-lobe injection of a hydrolysis-resistant cAMP analogue also depolarized ventral photoreceptors. Further work will be needed to resolve the role of cGMP in Limulus visual transduction.