Following Regulation, Imidacloprid Persists and Flupyradifurone Increases in Nontarget Wildlife.

After regulation of pesticides, determination of their persistence in the environment is an important indicator of effectiveness of these measures. We quantified concentrations of two types of systemic insecticides, neonicotinoids (imidacloprid, acetamiprid, clothianidin, thiacloprid, and thiamethoxam) and butenolides (flupyradifurone), in off-crop nontarget media of hummingbird cloacal fluid, honey bee (Apis mellifera) nectar and honey, and wildflowers before and after regulation of imidacloprid on highbush blueberries in Canada in April 2021. We found that mean total pesticide load increased in hummingbird cloacal fluid, nectar, and flower samples following imidacloprid regulation. On average, we did not find evidence of a decrease in imidacloprid concentrations after regulation. However, there were some decreases, some increases, and other cases with no changes in imidacloprid levels depending on the specific media, time point of sampling, and site type. At the same time, we found an overall increase in flupyradifurone, acetamiprid, thiamethoxam, and thiacloprid but no change in clothianidin concentrations. In particular, flupyradifurone concentrations observed in biota sampled near agricultural areas increased twofold in honey bee nectar, sevenfold in hummingbird cloacal fluid, and eightfold in flowers after the 2021 imidacloprid regulation. The highest residue detected was flupyradifurone at 665 ng/mL (parts per billion [ppb]) in honey bee nectar. Mean total pesticide loads were highest in honey samples (84 ± 10 ppb), followed by nectar (56 ± 7 ppb), then hummingbird cloacal fluid (1.8 ± 0.5 ppb), and least, flowers (0.51 ± 0.06 ppb). Our results highlight that limited regulation of imidacloprid does not immediately reduce residue concentrations, while other systemic insecticides, possibly replacement compounds, concurrently increase in wildlife. Environ Toxicol Chem 2024;43:1497-1508. © 2024 The Authors. Environmental Toxicology and Chemistry published by Wiley Periodicals LLC on behalf of SETAC.

Migration and non-breeding ecology of the Yellow-breasted Chat Icteria virens.

Detailed information spanning the full annual cycle is lacking for most songbird populations. We examined breeding, migration, and non-breeding sites for the Yellow-breasted Chat (Icteria virens, chat). We deployed archival GPS tags and light-level geolocators on breeding chats in British Columbia and light-level geolocators in California from 2013 to 2017 to determine migration routes and non-breeding sites. We examined whether chats overwintered in protected areas and characterized the percent of land cover within 1 km. We used a combination of genetics and stable hydrogen isotopes from feathers collected on non-breeding chats in Nayarit, Mexico (2017-2019) and migrating chats in Chiapas, Mexico (2018) and Veracruz, Mexico (2014-2015) to determine subspecies and infer breeding location. Endangered chats in British Columbia followed the Pacific Flyway and spent the non-breeding period in Sinaloa and Nayarit, Mexico. Two out of five chats spent the non-breeding period in protected areas, and the most common landcover type used was tropical or subtropical broadleaf deciduous forest. We found no mixing of eastern and western chats in our Mexico sites, suggesting strong migratory connectivity at the subspecies level. Western chats likely originating from multiple breeding latitudes spent the non-breeding period in Nayarit. Eastern Yellow-breasted Chats likely breeding across various latitudes migrated through Veracruz and Chiapas. Our results provide precise migration routes and non-breeding locations, and describe habitat cover types for chats, notably an endangered population in British Columbia, which may be valuable for habitat protection and conservation efforts. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s10336-021-01931-8.

s-ketamine enhances thalamocortical and corticocortical synaptic transmission in acute murine brain slices via increased AMPA-receptor-mediated pathways.

Despite ongoing research efforts and routine clinical use, the neuronal mechanisms underlying the anesthesia-induced loss of consciousness are still under debate. Unlike most anesthetics, ketamine increases thalamic and cortical activity. Ketamine is considered to act via a NMDA-receptor antagonism-mediated reduction of inhibition, i.e., disinhibition. Intact interactions between the thalamus and cortex constitute a prerequisite for the maintenance of consciousness and are thus a promising target for anesthetics to induce loss of consciousness. In this study, we aim to characterize the influence of s-ketamine on the thalamocortical network using acute brain-slice preparation. We performed whole-cell patch-clamp recordings from pyramidal neurons in cortical lamina IV and thalamocortical relay neurons in acute brain slices from CB57BL/6N mice. Excitatory postsynaptic potentials (EPSPs) were obtained via electrical stimulation of the cortex with a bipolar electrode that was positioned to lamina II/III (electrically induced EPSPs, eEPSPs) or via optogenetic activation of thalamocortical relay neurons (optogenetically induced EPSPs, oEPSPs). Intrinsic neuronal properties (like resting membrane potential, membrane threshold for action potential generation, input resistance, and tonic action potential frequency), as well as NMDA-receptor-dependent and independent spontaneous GABAA-receptor-mediated inhibitory postsynaptic currents (sIPSCs) were evaluated. Wilcoxon signed-rank test (level of significance < 0.05) served as a statistical test and Cohen's U3_1 was used to determine the actual effect size. Within 20 min, s-ketamine (5 µM) significantly increased both intracortical eEPSPs as well as thalamocortical oEPSPs. NMDA-receptor-mediated intracortical eEPSPs were significantly reduced. Intrinsic neuronal properties of cortical pyramidal neurons from lamina IV and thalamocortical relay neurons in the ventrobasal thalamic complex were not substantially affected. Neither a significant effect on NMDA-receptor-dependent GABAA sIPSCs (thought to underly a disinhibitory effect) nor a reduction of NMDA-receptor independent GABAA sIPSCs was observed. Both thalamocortical and intracortical AMPA-receptor-mediated EPSPs were significantly increased.In conclusion, our findings show no evidence for a NMDA-receptor antagonism-based disinhibition, but rather suggest an enhanced thalamocortical and intracortical synaptic transmission, which appears to be driven via increased AMPA-receptor-mediated transmission.