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. 2011 Mar;162(5):1083–1095. doi: 10.1111/j.1476-5381.2010.01108.x

Figure 7.

Figure 7

Proposed model for cyclic nucleotide-dependent signalling of growth cone collapse in adult autonomic neurones in response to Sema3A. In parasympathetic neurones, Sema3A binds to Nrp-1 and activates adenylyl cyclase, leading to the production of cAMP. In turn, cAMP activates PKA, which mediates growth cone collapse. However, cGMP may positively regulate growth cone dynamics independent of Sema3A signalling, since inhibition of PKG caused collapse. In sympathetic neurones, Sema3A binds Nrp-1 and stimulates cGMP production via soluble guanylyl cyclase. In turn, cGMP preferentially activates cyclic nucleotide-gated channels (CNGCs) (1), which mediate growth cone collapse. However, if CNGCs are inhibited, cGMP activates PKG (2), which does not cause collapse. Growth cone collapse is also caused by cAMP in sympathetic neurones, but this occurs independently of Sema3A and PKA signalling. AC, adenylyl cyclase; CNGCs, cyclic nucleotide-gated ion channel; Nrp-1, neuropilin-1; PKA, protein kinase A; PKG, protein kinase G; Sema3A, semaphorin 3A; sGC, soluble guanylyl cyclase.