| Research Abstract |
1. Horizontal cells in carp and turtle retinas are electrically coupled through gap junctions, and the input resistance of the cells is too low to be measured. However, the input resistance was significantly increased after injection of L-arginine, known as the precursor of nitric oxide (NO), or arachidonic acid into horizontal cells. Intracellular injection of these chemicals also blocked dye-coupling of Lucifer Yellow CH among horizontal cells.
2. On the other hand, dye-coupling was observed when the mixture of L- arginine and an NO synthase inhibitor, such as N^G-monomethyl-L-arginine and N^G-nitro-L-arginine, was injected into horizontal cells. Injection of a soluble guanylate cyclase inhibitor, such as methylene blue and cystamine, also suppressed the decoupling effect of L-arginine.
3. Dye-coupling was observed when nordihydroguaiaretic acid (NDGA), a lipoxygenase inhibitor, was injected into the cells, together with arachidonic acid. Injection of methylene blue or cystamine also suppressed the decoupling effect of arachidonic acid. On the other hand, dye-coupling was eliminated when indomethacin, a cyclo-oxygenase inhibitor, was injected into horizontal cells, together with arachidonic acid. And injection of the mixture of arachidonic acid and indomethacin caused significant increase in the input resistance of horizontal cells.
4. These results suggest that nitric oxide (NO) and lipoxygenase metabolites of arachidonic acid block gap junctions between retinal neurons, and that the decoupling effects are induced by activating guanylate cyclase.
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