To better understand the olfactory mechanisms in the two lepidopteran pest model species, the Helicoverpa armigera and H. assulta, we conducted transcriptome analysis of the adult antennae using Illumina sequencing technology and compared the chemosensory genes between these two related species. Combined with the chemosensory genes we had identified previously in H. armigera by 454 sequencing, we identified 133 putative chemosensory unigenes in H. armigera including 60 odorant receptors (ORs), 19 ionotropic receptors (IRs), 34 odorant binding proteins (OBPs), 18 chemosensory proteins (CSPs), and 2 sensory neuron membrane proteins (SNMPs). Consistent with these results, 131 putative chemosensory genes including 64 ORs, 19 IRs, 29 OBPs, 17 CSPs, and 2 SNMPs were identified through male and female antennal transcriptome analysis in H. assulta. Reverse Transcription-PCR (RT-PCR) was conducted in H. assulta to examine the accuracy of the assembly and annotation of the transcriptome and the expression profile of these unigenes in different tissues. Most of the ORs, IRs and OBPs were enriched in adult antennae, while almost all the CSPs were expressed in antennae as well as legs. We compared the differences of the chemosensory genes between these two species in detail. Our work will surely provide valuable information for further functional studies of pheromones and host volatile recognition genes in these two related species.

Nitric oxide (NO) has only recently been appreciated as a normal biologic substance with a role in signal transduction. It was first identified as endothelial-derived relaxing factor in blood vessels and as the mediator of the tumoricidal and bactericidal actions of macrophages. NO's role as a neural messenger may be even more prominent. Biosynthesis of NO involves oxidation of the guanidine group of arginine with stoichiometric formation of citrulline. NO synthase is one of the most extensively regulated enzymes in biology. In the periphery, NO is a likely transmitter of nonadrenergic, noncholinergic neurons. In the brain, NO neurons mediate action of glutamate acting at N-methyl-D-aspartate (NMDA) receptors. Excess release of NO appears to account for a major portion of neural damage following vascular stroke.