Insecticide exposure during brood or early-adult development reduces brain growth and impairs adult learning in bumblebees.
Ontology highlight
ABSTRACT:
SUBMITTER: Smith DB
PROVIDER: S-EPMC7126076 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Widespread use of neonicotinoid insecticides, such as imidacloprid, is often associated with diminishing populations of bees; this loss of pollinators presents a concern for food security and may cause unpredictable changes in ecological networks. However, little is known about the potential behavioural mechanisms behind the neonicotinoid-associated pollinator decline. We quantified the effects of low-dose (1 ppb) imidacloprid exposure on the foraging behaviour of bumblebees (Bombus terrestris). Individual bumblebees were released into a flight arena containing three patches of robotic flowers whose colour (yellow, orange, blue) indicated whether the flower delivered a reward (sugar solution). Exposure to imidacloprid had no significant effect on measures of bumblebee physical performance (such as flight speed) or learning (identifying rewarding flowers). However, pesticide-treated bumblebees had reduced foraging motivation compared with the control bumblebees, as they visited fewer robotic flowers, were slower to start foraging and did not visit all three flower colours as often. Neonicotinoid concentrations of 1 ppb, often reported in plant nectar near agricultural lands, can thus affect the foraging behaviour of bumblebees. Even without a notable impact on flight performance and learning, a reduction in foraging motivation could explain the poor performance of colonies of bumblebees exposed to neonicotinoids.
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Project description:Ketamine exposure can lead to selective neuroapoptosis in the developing brain. p66ShcA, the cellular adapter protein expressed selectively in immature neurons, is a known pro-apoptotic molecule that triggers neuroapoptosis when activated. Sprague-Dawley rats at postnatal day 7 were subcutaneously injected in the neck with ketamine 20 mg/kg, six times at 2-hour intervals. At 0, 1, 3, and 6 hours after final injection, western blot assay was used to detect the expression of cleaved caspase-3, p66ShcA, and phosphorylated p66ShcA. We found that the expression of activated p66ShcA and caspase-3 increased after ketamine exposure and peaked at 3 hours. The same procedure was performed on a different group of rats. At the age of 4 weeks, spatial learning and memory abilities were tested with the Morris water maze. Latency to find the hidden platform for these rats was longer than it was for control rats, although the residence time in the target quadrant was similar. These findings indicate that ketamine exposure resulted in p66ShcA being activated in the course of an apoptotic cascade during the neonatal period. This may have contributed to the deficit in spatial learning and memory that persisted into adulthood. The experimental protocol was approved by the Institutional Animal Care and Use Committee at the University of Texas at Arlington, USA (approval No. A13.008) on January 22, 2013.
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Project description:Recent concern over global pollinator declines has led to considerable research on the effects of pesticides on bees. Although pesticides are typically not encountered at lethal levels in the field, there is growing evidence indicating that exposure to field-realistic levels can have sublethal effects on bees, affecting their foraging behaviour, homing ability and reproductive success. Bees are essential for the pollination of a wide variety of crops and the majority of wild flowering plants, but until now research on pesticide effects has been limited to direct effects on bees themselves and not on the pollination services they provide. Here we show the first evidence to our knowledge that pesticide exposure can reduce the pollination services bumblebees deliver to apples, a crop of global economic importance. Bumblebee colonies exposed to a neonicotinoid pesticide provided lower visitation rates to apple trees and collected pollen less often. Most importantly, these pesticide-exposed colonies produced apples containing fewer seeds, demonstrating a reduced delivery of pollination services. Our results also indicate that reduced pollination service delivery is not due to pesticide-induced changes in individual bee behaviour, but most likely due to effects at the colony level. These findings show that pesticide exposure can impair the ability of bees to provide pollination services, with important implications for both the sustained delivery of stable crop yields and the functioning of natural ecosystems.
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Project description:Sulfoximine-based insecticides, such as sulfoxaflor, are of increasing global importance and have been registered for use in 81 countries, offering a potential alternative to neonicotinoid insecticides.Previous studies have demonstrated that sulfoxaflor exposure can have a negative impact on the reproductive output of bumblebee colonies, but the specific life-history variables that underlie these effects remain unknown.Here, we used a microcolony-based protocol to assess the sub-lethal effects of chronic sulfoxaflor exposure on egg laying, larval production, ovary development, sucrose consumption, and mortality in bumblebees. Following a pre-registered design, we exposed colonies to sucrose solutions containing 0, 5, 10 and 250ppb of sulfoxaflor. Exposure at 5 ppb has been previously shown to negatively impact colony reproductive success.Our results showed that sulfoxaflor exposure at 5 ppb (lowest exposure tested) reduced the number of eggs found within the microcolonies (Hedge's d = -0.37), with exposed microcolonies also less likely to produce larvae (Hedge's d = -0.36). Despite this, we found no effect of sulfoxaflor exposure on ovarian development. Sulfoxaflor-exposed bumblebees consumed less sucrose solution, potentially driving the observed reduction in egg laying. Policy implications. Regulatory bodies such as the European Food Safety Authority (EFSA) are under increasing pressure to consider the potential impact of insecticides on wild bees, such as bumblebees, but sublethal effects can go undetected at lower-tier testing. In identifying just such an effect for bumblebees exposed to sulfoxaflor, this study highlights that microcolony-based protocols are a useful tool that could be implemented within an ecotoxicology framework. Furthermore, the results provide evidence for potentially negative consequences of pollinator exposure to an insecticide that is currently undergoing the licensing process in several EU member states.
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Project description:Exposure to early life trauma (ELT) is known to have a profound impact on mental development, leading to a higher risk for depression and anxiety. Our aim was to use multiple structural imaging methods to systematically investigate how traumatic stressors early in life impact the emotional brain circuits, typically found impaired with clinical diagnosis of depression and anxiety, across the lifespan in an otherwise healthy cohort. MRI data and self-reported histories of ELT from 352 healthy individuals screened for no psychiatric disorders were analyzed in this study. The volume and cortical thickness of the limbic and cingulate regions were assessed for all participants. A large subset of the cohort also had diffusion tensor imaging data, which was used to quantify white matter structural integrity of these regions. We found a significantly smaller amygdala volume and cortical thickness in the rostral anterior cingulate cortex associated with higher ELT exposure only for the adolescence group. White matter integrity of these regions was not affected. These findings demonstrate that exposure to early life trauma is associated with alterations in the gray matter of cingulate-limbic regions during adolescence in an otherwise healthy sample. These findings are interesting in the context that the affected regions are central neuroanatomical components in the psychopathology of depression, and adolescence is a peak period for risk and onset of the disorder.
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Project description:Neonicotinoids are widely-used pesticides implicated in the decline of bees, known to have sub-lethal effects on bees' foraging and colony performance. One proposed mechanism for these negative effects is impairment to bees' ability to learn floral associations. However, the effects of neonicotinoids on learning performance have largely been addressed using a single protocol, where immobilized bees learn an association based on a single sensory modality. We thus have an incomplete understanding of how these pesticides affect bee learning in more naturalistic foraging scenarios. We carried out the first free-foraging study into the effects of acute exposure of a neonicotinoid (imidacloprid) on bumblebees' (Bombus impatiens) ability to learn associations with visual stimuli. We uncovered dose-dependent detrimental effects on motivation to initiate foraging, amount of nectar collected, and initiation of subsequent foraging bouts. However, we did not find any impairment to bees' ability to learn visual associations. While not precluding the possibility that other forms of learning are impaired, our findings suggest that some of the major effects of acute neonicotinoid exposure on foraging performance may be due to motivational and/or sensory impairments. In light of these findings, we discuss more broadly how pesticide effects on pollinator cognition might be studied.
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