Nitric oxide modulation of the electrically excitable skin of Xenopus laevis frog tadpoles.

Nitric oxide (NO) is a highly diffusible signalling molecule with widespread effects on the integrative electrical properties of a variety of neuronal and muscle cells. We have explored the effects of NO on the cardiac-like impulse generated by skin cells of the hatchling Xenopus tadpole. Skin cell impulses propagate from cell to cell via gap junctions and form an unusual sensory system, which triggers escape behaviour at early stages of amphibian development. We show that the NO donor S-nitroso-N-acetylpenicillamine (SNAP) increases the duration of the skin impulse and slows the rate of impulse propagation across the skin, and also produces a significant depolarization of the membrane potential of skin cells. Each of these effects of SNAP is significantly reversed by the NO scavenger, C-PTIO. Possible sources of NO have been investigated using both NADPH-diaphorase histochemistry and nNOS immunocytochemistry to label the enzyme nitric oxide synthase (NOS), and DAF-2 to label NO itself. In each case a punctate distribution of skin cells is labelled, indicating that the endogenous production of NO may regulate the properties of the skin impulse.