Figure 3.

Modulation of the nitric oxide signaling pathway has no effect on OSN response. (A) Schema of the nitric oxide signaling pathway. Activation of nitric oxide synthase (NOS) induces nitric oxide (NO) production. In turn, NO activates soluble guanyl cyclase-dependent catalysis of GTP into cGMP, which is hypothesized to induce non-selective channel opening of Orco. Various agents (blue) can be used to modulate the signaling pathway. NO signaling leads to increased production of the cyclic nucleotide cGMP. cGMP in turn acts on cyclic nucleotide-gated ion channels (CNG), regulates cGMP-dependent protein kinases (cGK), and gets degraded by specific phosphodiesterases (PDE). (B) Time course of OSN responses to VUAA1 in the absence (first response) and presence (second response) of 10 μM ODQ, a highly selective and irreversible inhibitor of soluble guanyl cyclase. The bar plot indicates the mean total response amplitude for each response ± SEM. (C) Time course of OSN responses in the absence (first response) and presence (second response) of 10 μM sodium nitroprusside (SNP), a potent nitric oxide donor functioning as an activator of soluble guanyl cyclase. The bar plot indicates the mean total response amplitude for each response ± SEM. (D) Time course of OSN responses in the absence (first response) and presence (second response) of 10 μM L-NAME, a nitric oxide synthase inhibitor. The bar plot indicates the mean total response amplitude for each response ± SEM. Peak response latencies are reported in parentheses in all bar plots.