Monosodium glutamate, (MSG) an amino acid eliciting umami gustatory response in animals, increases leaf consumption and accelerates feeding initiation in neonatal larvae of codling moth (Cydia pomonella). MSG was successfully employed as an additive increasing efficacy of per os- acting insecticides. However, as a highly water soluble substance, MSG works best only under no-rain conditions. Here, L-Aspartic acid, (L-Asp) a less water-soluble amino acid was tested. Additionally, we investigated proximate cellular mechanisms responsible for transduction of the feeding stimulus from L-Asp in codling moth neonates.

L- Asp alone accelerated feeding commencement in codling moth neonates. Addition of phospholipase C inhibitor, U73122, to L-Asp did not reverse feeding stimulatory properties of the latter; feeding commenced after the same time in larvae exposed to L-Asp alone and those exposed to L-Asp in combination with U73122 Addition of adenylate cyclase activator NHK 477, or phosphodiesterase inhibitor Rolipram, abolished stimulatory effect of L-Asp on feeding commencement. The latter result suggests L-Asp induces feeding in codling moth neonates via c-AMP dependent pathway, similar to MSG.

Leaf consumption increased with the application of L-Asp. This stimulatory effect was not affected by MK-801, a blocker of vertebrate NMDA glutamate receptors. Feeding stimulatory effects of L-Asp also remained unaffected by withdrawal of calcium from foliage with EDTA, indicating that effects of L-Asp on feeding intensity in codling moth neonates are not mediated by NMDA-like ionotropic glutamate receptors. D-Asp had no effect on time of feeding commencement or foliage consumption by codling moth larvae