The battle between plants and phytophagous insects has lasted for hundreds of millions of years. Over time, plants have evolved sophisticated defence systems to counteract attacks from insects. After being attacked by herbivores, plants quickly generate herbivory-specific signals, and, through complicated networks, these signals then trigger large-scale biochemical and physiological changes. The success of plants in withstanding herbivore attacks depends on their ability to quickly recognize elicitors in insect regurgitant. When herbivorous insects feed on plants, their regurgitant inevitably comes in contact with the wounded plant tissue. Thereby, the insects provide chemical signals that might be involved in the interaction between the attacking insect and the defending plant. In general, the earliest detectable signalling events in plants defence responses include transmembrane ion fluxes and production of reactive oxygen species. In plant cells, the calcium ion is a ubiquitous intracellular second messenger involved in numerous signalling pathways. It is widely acknowledged that calcium flux across cellular membranes plays a key role in triggering and mediating defence mechanisms. Hydrogen peroxide is a common component of the defence responses of plants against herbivore attacks. The non-invasive microelectrode ion flux measurement technique, which can monitor ion/molecule-specific activities non-disruptively, has become a popular tool for studying adaptive responses of plant cells and tissues to a large number of abiotic stresses. Using a non-invasive micro-test system and a confocal laser scanning microscope, Ca²⁺ influx and variation in hydrogen peroxide production induced by the regurgitant of Orgyia ericae Germar were investigated in Ammopiptanthus mongolicus (Maxim. ex Kom.) Cheng f. cells. Experiments were conducted in the Key Laboratory of Forest Silviculture of the State Forestry Administration from June 2010 to April 2011. The results showed that Ca²⁺ influx and hydrogen peroxide accumulation were induced by the regurgitant, indicating that Ca²⁺ influx and variation in hydrogen peroxide production were early signalling events in response to the regurgitant. Ca²⁺ influx was incompletely inhibited by the Ca²⁺ channel blocker GdCl₃, demonstrating that the Ca²⁺ channel on the plasma membrane was not the only route of Ca²⁺ into the cell. Alamethicin, a voltage-gated ion channel-forming peptide mixture derived from the soil fungus Trichoderma viride Pers., induced Ca²⁺ influx, but this alamethicin-induced Ca²⁺ influx was not inhibited by the Ca²⁺ channel blocker GdCl₃. These results provided indirect evidence that one or more components of regurgitant exhibited ion channel-forming activities in the cell plasma membrane, and that the activity of those channels was not inhibited by GdCl₃. Hydrogen peroxide accumulation was completely inhibited by the extracellular calcium chelator EGTA, but GdCl₃ incompletely inhibited hydrogen peroxide production, demonstrating that Ca²⁺ influx was necessary for the production of hydrogen peroxide. Some compounds in oral secretions from O. ericae induced NADPH oxidase activity. The application of regurgitant from O. ericae resulted in immediate and rapid hydrogen peroxide accumulation. The accumulation of hydrogen peroxide in cells in response to the regurgitant of O. ericae was inhibited by the NADPH oxidase inhibitor diphenylene iodonium, demonstrating that hydrogen peroxide was primarily generated from the activation of NADPH oxidase on the plasma membrane.