Spiders are among the most abundant predators of insects and other invertebrates in agro-and forest ecosystems, playing an important ecological role by regulating invertebrate populations. Biological control using spiders may represent a sustainable method of controlling agricultural pest species and reducing the amount of pest damage on crops. However, pesticide application on agricultural crops may directly or indirectly impact spider foraging in the crop. In particular, pesticides may have mutagenic effects on spiders, negatively affecting the spider population abundance and transferring these effects to the next generation. Recent studies have reported that low-dose pesticides kill pests, but promote the predation of natural enemies. Therefore, revealing the mechanism behind low-dose pesticides on natural enemies is critical to improving predator ability, exploring the potential control of insect predators and coordinating bio-and chemical control. Our aim was to investigate the effect of low-dose pesticides on spider predation behavior and reveal the underlying mechanisms. Pardosa astrigera was treated with a low-dose of imidacloprid using the drug-film method. We determined the sensitivity of P. astrigera, the predation effect of P. astrigera on B. brassicae and the activity of acetylcholinesterase (AChE), glutathione S-transferase (GSTs), superoxide dismutase (SOD), catalase (CAT) and midgut proteinase. The results showed that under different concentrations of imidacloprid, the predacious functional response of spiders on aphids belonged to the Holling type. Compared with the control, the theoretical maximal consumption increased, searching efficiency decreased and the prey handling time declined with increasing aphid density. Therefore, low-dose pesticide levels resulted in enhanced predation by spiders. When P. astrigera was treated with a low-dose of pesticide, this species showed a reduction in AChE and GSTs activity compared with the control (P<0.05), suggesting spider activity was inhibited. The inhibition was enhanced with increasing pesticide concentration and weakened with prolonged treatment. SOD, CAT and midgut proteinase activity were induced significantly at the low-dose of 1, 3 and 5mg/ L(P<0.050, but decreased gradually with increased concentration and extended treatment, with activity close to the control. After low-dose pesticide treatment, P. astrigera showed inhibited AChE activity, leading to reduced AChE sensitivity, less decomposition of AChE in nerve transfer and increased spider activity. Increased GSTs, SOD and CAT activity induced by low-dose pesticide, accelerated the spiders′metabolism, stimulating predatory behavior. Enhanced midgut proteinase activity may benefit food digestion and nutrient absorption. The low-dose pesticide regime may enhance the predatory behavior of P. Astrigera via three main pathways. First, it enhances the instant attack rate, shortens prey handling time and increases the amount of prey per day. Second, it affects physiological enzyme activity, inhibits to a degree the metabolic detoxification enzyme subject of: low doses of imidacloprid causing a reduction in AChE sensitivity of the neurotransmitter acetylcholine decomposition, resulting in higher spider excitability; increased protection enzyme, such as GSTs, SOD, CAT, function oxidases (MFOs) and esterase, resulting in the acceleration of spider metabolism, stimulating predator behavior. Third, on the physiological activity of digestive enzymes, low doses of pesticides activate protein midgut digestive enzymes, improving the digestion and absorption function of prey. In summary, certain concentrations of pesticide promote the predation function of P. astrigera against prey, changing spider behavior through a series of physiological and biochemical reactions.
CITATION STYLE
Li, R., Li, N., Liu, J., Li, S. C., & Hong, J. P. (2014). The effect of low-dose of pesticide on predation of spider and its preliminary mechanisms. Shengtai Xuebao/ Acta Ecologica Sinica, 34(10), 2629–2637. https://doi.org/10.5846/stxb201307241940
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