Sub-lethal neonicotinoid exposure impairs homing ability in honey bee (Apis mellifera) foragers via the disruption of energy metabolism and endocrine regulation rather than cognitive ability

초록

Neonicotinoid insecticides have been widely used in agriculture for pest control but pose significant risks to nontarget pollinators such as honey bees (Apis mellifera). While neonicotinoids, such as imidacloprid (IMI), have been banned for outdoor use in the European Union due to their environmental risks, they are still employed in many other countries for agricultural purposes. In the present study, we examined the impact of the neonicotinoids acetamiprid (ACE) and IMI on the homing ability of forager bees. Although both insecticides upregulated foraging-related genes, the return rate for treated bees significantly declined, particularly in the IMItreated group. Gene expression profiling revealed the downregulation of insulin/insulin-like signaling pathway components and mitochondrial respiration genes, indicating impaired energy metabolism. Furthermore, the expression of the gene encoding antioxidant enzymes, which act as surrogate markers of oxidative stress, was also downregulated, potentially reflecting suppressed mitochondrial respiration. The concurrent upregulation of a juvenile hormone-related gene and vitellogenin gene suggested that endocrine dysregulation may disrupt behavioral maturation and caste transitions. These results indicate that impaired homing performance following neonicotinoid exposure is not due to deficits in cognitive gene activation but is instead linked to systemic physiological disruptions involving energy depletion and hormonal imbalances. Our findings highlight the need for holistic risk assessments that consider the effects of sub-lethal pesticide exposure on pollinator health and colony sustainability.

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