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1 ion products that include a pyrethroid and a neonicotinoid.
2 th conjugated and hydrophobic regions of the neonicotinoid.
3 because it appears safer for honey bees than neonicotinoids.
4 ributions to the distinctive interactions of neonicotinoids.
5 ammals confer remarkable selectivity for the neonicotinoids.
6 arly vulnerable to the neurotoxic effects of neonicotinoids.
7 nt alkaloid nicotine and cross-resistance to neonicotinoids a class of synthetic insecticides widely
8 ebate about the environmental risks posed by neonicotinoids, a group of widely used, neurotoxic insec
9 ) fed field levels [10 nM, 2.1 ppb (w/w)] of neonicotinoid accumulate between 4 and 10 nM in their br
10 s exposed to different concentrations of the neonicotinoids acetamiprid, clothianidin, imidacloporid,
11 ticides by number and world market value are neonicotinoids acting as nAChR agonists or organophospho
13 stration that acute or chronic exposure to a neonicotinoid alone can significantly alter bee flight.
14 BRT) analysis to predict both probability of neonicotinoid analytical detection and concentration.
15 s [i.e., Lymnaea stagnalis (Ls) AChBP of low neonicotinoid and high nicotinoid sensitivities and Aply
18 ic exposure of bumblebees to two pesticides (neonicotinoid and pyrethroid) at concentrations that cou
19 f differential molecular recognition for the neonicotinoids and classical nicotinoids by estimates of
20 s at environmental realistic levels of three neonicotinoids and nicotine, and compared laboratory stu
22 proposed very different interactions of the neonicotinoids and nicotinoids might be examined with a
23 lision-induced dissociation analysis for the neonicotinoids and nicotinoids with similar labeling fre
25 gate the real-world links between the use of neonicotinoids and pollinator mortality are lacking.
26 (organophosphates, carbamates, pyrethroids, neonicotinoids, and manganese fungicides) and five indiv
28 ount for the cognitive impairments caused by neonicotinoids, and predict that exposure to multiple pe
29 r: throughout spring and summer, mixtures of neonicotinoids are also found in the pollen and nectar o
39 s, does not apply to the anomalous action of neonicotinoids at the insect nicotinic acetylcholine rec
40 dels based on AChBP directly map the elusive neonicotinoid binding site and further describe the mole
41 of the insect and mammalian nAChRs and their neonicotinoid-binding site lays the foundation for conti
43 s on the nicotinic receptor structure in the neonicotinoid-bound state revealed a unique niche of abo
45 nated nectar and pollen from treated plants, neonicotinoids can affect foraging, learning, and memory
48 nvironmental release of particles containing neonicotinoids can produce high exposure levels for bees
50 rcially with either seed coatings containing neonicotinoids (clothianidin or thiamethoxam) or no seed
52 Using Arabidopsis thaliana, we show that the neonicotinoid compounds, imidacloprid (IMI) and clothian
54 vels were generally not well correlated with neonicotinoid concentrations in flowers, pollen, or nect
55 14, respectively, calculated on the basis of neonicotinoid concentrations in preplant soil and seed a
57 the observed inability of shredders to avoid neonicotinoid-contaminated leaves, our results emphasize
58 gative relationship between honey and pollen neonicotinoid contamination and Apis colony weight gain.
59 r results suggest that sub-lethal effects of neonicotinoids could scale up to cause losses of bee bio
60 models effectively predicted the deviance in neonicotinoid detection (62.4%) and concentration (74.7%
64 the potent and selective interaction of the neonicotinoid electronegative pharmacophore with a uniqu
68 tion, but we present the first evidence that neonicotinoid exposure alone can impair the physical abi
69 l behavioral studies showed the link between neonicotinoid exposure and adverse effects on foraging a
70 This study examines the connection between neonicotinoid exposure and innate immune function in the
71 immune function in bumblebees is affected by neonicotinoid exposure and suggest a physiological mecha
72 -mitigation efforts should focus on reducing neonicotinoid exposure in the early spring when colonies
73 not provide spatial or temporal relief from neonicotinoid exposures in agricultural regions where th
74 Vitellogenin showed a strong increase upon neonicotinoid exposures in the laboratory and field, whi
75 pesticide that is reported to be safer than neonicotinoids for honey bees, thus deserve greater atte
79 Here we show that sublethal doses of the neonicotinoid imidacloprid impair sexual communication a
80 laboratory to field-realistic levels of the neonicotinoid imidacloprid, then allowed them to develop
81 ly isolated honeybee brain, we show that the neonicotinoids imidacloprid and clothianidin, and the or
83 pression is similarly induced by a different neonicotinoid, imidacloprid, but not by the organophosph
86 selected organophosphates, pyrethroids, and neonicotinoids in seven Indian field populations of Bemi
89 , these chloropyridinyl- and chlorothiazolyl-neonicotinoids induce SA responses associated with enhan
91 repeated pulses of low concentrations of the neonicotinoid insecticide (thiacloprid) continuously dec
93 Imidacloprid (IMD) is the most widely used neonicotinoid insecticide found on environmental surface
94 re assessed for their sensitivity toward the neonicotinoid insecticide thiacloprid using their feedin
95 a, we show that (i) eight metabolites of the neonicotinoid insecticide, imidacloprid, can be detected
96 o field-realistic levels of a widely applied neonicotinoid insecticide, thiamethoxam, on bumblebee od
99 black alder trees treated with one of three neonicotinoid insecticides (imidacloprid, thiacloprid, o
103 were achieved rivaling those of the current neonicotinoid insecticides as illustrated here by 3-(6-c
104 n Commission has restricted the use of three neonicotinoid insecticides as seed dressings on bee-attr
108 impact of pathogens in honey bees exposed to neonicotinoid insecticides has been reported, but the ca
114 the negatively charged (delta(-)) tip of the neonicotinoid insecticides interacts with a putative cat
119 cent efforts to evaluate the contribution of neonicotinoid insecticides to worldwide pollinator decli
120 ate the potential exposure of pollinators to neonicotinoid insecticides used as seed treatments on co
123 s and also toxicants such as epibatidine and neonicotinoid insecticides with a chloropyridinyl substi
124 ney bees tested positive for the presence of neonicotinoid insecticides, and there was only one trace
125 posure of honeybees to and intoxication with neonicotinoid insecticides, namely, the atmospheric emis
131 e negatively tipped ("magic" nitro or cyano) neonicotinoids interact with a proposed unique subsite c
135 overlapped with those related to exposure to neonicotinoids, like the polyamine metabolism involved i
136 sents a rarely studied pathway through which neonicotinoids may enter nontarget environments, e.g., s
137 d suggest a physiological mechanism by which neonicotinoids may impact the innate immune function of
138 havior and improves our understanding of how neonicotinoids may impair short-term colony functioning.
140 iral proliferation suggests that the studied neonicotinoids might have a negative effect at the field
141 and selectivity are retained when the usual neonicotinoid N-nitroimine (=NNO(2)) electronegative tip
142 studies have identified detectable levels of neonicotinoids (neonics) in the environment, adverse eff
143 idely used classes of cholinergic pesticide: neonicotinoids (nicotinic receptor agonists) and organop
144 idine (1), were used to probe the Drosophila neonicotinoid-nicotinic acetylcholine receptor interacti
146 us, sublethal cognitive deficits elicited by neonicotinoids on a broad range of native bee species de
147 ng-term exposure and suggest that impacts of neonicotinoids on olfaction are greater than their effec
149 ss well studied are the potential effects of neonicotinoids on queen bees, which may be exposed indir
155 the impacts of field-realistic exposure to a neonicotinoid pesticide may seriously compromise this im
159 s can pose environmental risks, and a common neonicotinoid pesticide, thiamethoxam, decreases homing
163 tions containing field-relevant doses of the neonicotinoid pesticides, imidacloprid (IMD) and thiamet
164 position is a key indicator and/or driver of neonicotinoid presence and concentration in Prairie wetl
165 biotic wetland characteristics likely affect neonicotinoid presence and environmental persistence, bu
166 -substituted guanidine/amidine planes of the neonicotinoids provide a unique electronic conjugation s
171 ecological and agronomic factors underlying neonicotinoid residues is needed to inform evidence-base
172 residues were used to differentiate between neonicotinoid residues originating from seed or from dis
173 To estimate risk posed by this pathway, neonicotinoid residues were analyzed in foliage from bla
175 en, and cotton nectar contained little or no neonicotinoids resulting from insecticide seed treatment
176 associated with the metabolic resistance to neonicotinoids, results in a significant increase in the
178 vide the first evidence that farmers who use neonicotinoid seed coatings reduce the number of subsequ
180 We hypothesize that any sublethal effects of neonicotinoid seed dressings on Bombus colonies are pote
182 s and Aplysia californica (Ac) AChBP of high neonicotinoid sensitivity] mimicking vertebrate and inse
184 take) associated with the systemic nature of neonicotinoids should be accounted for during their regi
185 es RKRIRRMMPRPS and RNRHTHLRTRPR for binding neonicotinoids such as thiacloprid and imidacloprid.
186 As an exception, the remarkably potent OP neonicotinoid synergist, O-propyl O-(2-propynyl) phenylp
187 via spray drift or surface runoff or (due to neonicotinoids' systemic nature) via senescent leaves.
189 es, the nicotinic acetylcholine receptor for neonicotinoids, the gamma-aminobutyric acid receptor/chl
191 at were either untreated or treated with the neonicotinoid thiacloprid as part of normal farming prac
192 s) colonies to field-realistic levels of the neonicotinoid thiamethoxam (2.4ppb & 10ppb) over four we
193 alistic, chronic exposure to the widely-used neonicotinoid thiamethoxam on the development of sonicat
194 at, spiromesifen and spirodiclofen) and five neonicotinoid (thiamethoxam, chlotianidin, imidacloprid,
195 thiacloprid, a widely used cyano-substituted neonicotinoid thought to be less toxic to honey bees and
196 af-shredding invertebrates may be exposed to neonicotinoids through both the water phase and the cons
198 abolizing P450) at metabolizing nicotine and neonicotinoids to less toxic metabolites in vitro and ge
199 getation be retained or restored to minimize neonicotinoid transport and retention in wetlands, there
201 ous field studies, leaving the net impact of neonicotinoid treated crops on bees relatively unknown.
202 e field experiments to assess the effects of neonicotinoid-treated crops on three bee species across
206 ny losses and national-scale imidacloprid (a neonicotinoid) usage patterns across England and Wales.
207 y targeted efforts could considerably reduce neonicotinoid use in field crops without yield declines
211 ble data to estimate and interpret trends in neonicotinoid use since their introduction in 1994, with
214 thereby establishing an atypical concept for neonicotinoid versus nicotinoid selectivity between inse
215 d removal of six high-production high-volume neonicotinoids was investigated in 13 conventional waste
216 NMI) analog of imidacloprid, a highly potent neonicotinoid, was used here as a radioligand, uniquely
219 e been based on the premise that exposure to neonicotinoids would occur only during the blooming peri
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