Cover legend: A labeled B2 buccal neuron of a pond snail (Lymnaea stagnalis) shows extensive neurite growth 2 d after axonal injury (top right) compared to a non-injured B2 neuron (top left). The injury-induced neurite growth strongly depends on endogenous nitric oxide (NO) production: inhibiting either NO synthase (middle left) or the NO receptor soluble guanylate cyclase (lower left) suppresses neurite growth. The effect of blocking NO production on neurite growth can be inhibited by coapplication of a NO donor (middle right), whereas blocking protein kinase G, which can act downstream of soluble guanylate cyclase (lower right) has no effect on neurite growth. For more information, see the article by Cooke et al. in this issue (pages 5626–5637).