Host: The Japanese Society of Toxicology
Multiple factors have been associated with the honey bee colony losses in the past 25 years. Accumulating evidence indicates that at sublethal doses, neonicotinoids cause honey bee brain dysfunction and reduce immunocompetence, leading to impaired navigation and olfactory learning and memory, and susceptibility to pathogens. Moreover, such pesticides disturb the reproductive system of queen bees, i.e., the number of eggs and viability of sperm stored in the spermatheca of queen bees, thereby reducing the numbers of adult bees and broods. Pesticide exposure during the larval development stages prolongs larval development and shortens adult longevity. In addition, the density of synaptic units in the calyces of mushroom bodies in the heads decreases; this effect has been further associated with the abnormal olfactory learning ability of adult honey bees exposed to sublethal doses of imidacloprid during the larval stage. Therefore, numerous physiological aspects of honey bees might be altered after exposure to pesticides at sublethal doses, regardless of the developmental stage. We evaluated the impact of the most widely used neonicotinoids—imidacloprid—on different developmental stages of honey bees by profiling the transcriptomes of worker bees with imidacloprid during only the larval stage. Our results confirm that even intaking 1 ppb imidacloprid during only the larval stage would be enough to severely impact a bee’s gene expression. The existence of many differentially expressed genes may reflect or result in honey bee disorder.
