Nitric oxide controls the light adaptive chromatic difference in receptive field size of H1 horizontal cell network in carp retina.

In carp retina, the receptive field size of the H1-type horizontal cell (HC) network is known to be chromatically selective, as electrophysiological signals are generated by short-wavelength (SW) light stimuli, which spread much less than those for long-wavelength (LW). We have shown previously that the signalling mechanism underlying this chromatic difference operates only in the light-adapted retina and that it involves cGMP as an intermediary messenger. In the present study, the possible role of nitric oxide (NO) as such a control mechanism was investigated. Application of a NO donor (SNP or SNOG) to dark-adapted retinae produced a chromatic difference in the receptive field size, such as in the light-adapted state. This effect was due mainly to a reduction in the spread of signals generated by SW stimuli; LW signalling spread was not altered. No such effect was observed in light-adapted retinae where a chromatic difference in receptive field size was already present. On the other hand, application of the NO 'scavenger' haemoglobin to light-adapted retinae suppressed the chromatic difference. These results are consistent with NO being a light-adaptive retinal neuromodulator involved in the generation of the chromatic difference in H1 cell receptive field size. These results are discussed in the context of two different hypotheses.