The role of Ins(1,4,5)P(3) in signal transduction of the metabolic neuropeptide Mem-CC in the cetoniid beetle,Pachnoda sinuata

We have investigated the role of inositol triphosphate, Ins(1,4,5)P₃, in the transduction of the hypertrehalosaemic and hyperprolinaemic signal of the endogenous neuropeptide Mem-CC in the cetoniid beetle Pachnoda sinuata. Flight and injection of Mem-CC into the haemocoel of the beetle induce an increase of Ins(1,4,5)P₃ levels in the fat body of the beetle. When Mem-CC is co-injected with U 73122, which is an inhibitor of phospholipase C, this effect is abolished. Mem-CC also elevates Ins(1,4,5)P₃ concentration in fat body pieces in vitro. The increase in Ins(1,4,5)P₃ levels is tissue-specific and does not occur in brain and flight muscles. Elevation of the Ins(1,4,5)P₃ levels upon injection of Mem-CC is time- and dose-dependent: the maximum response is reached after 3 min and a dose of 10 pmol is needed. Compounds that mimic the action of cAMP (cpt-cAMP, forskolin) do not influence the concentration of Ins(1,4,5)P₃, while those that stimulate G-proteins (aluminium fluoride and cholera toxin) cause an increase of Ins(1,4,5)P₃ levels. The application (in vivo and in vitro) of F-Ins(1,4,5)P₃, an Ins(1,4,5)P₃ analogue that penetrates the cell membrane, causes a mobilisation of carbohydrate reserves via the activation of glycogen phosphorylase but does not stimulate proline synthesis. In addition, U 73122 abolishes the hypertrehalosaemic but not the hyperprolinaemic effect of Mem-CC. The results suggest that the hypertrehalosaemic signal of Mem-CC is mediated via an increase of Ins(1,4,5)P₃ levels in the fat body of P. sinuata.