Showing papers by "James J L Hodge published in 2020"
TL;DR: Exposure to the field-relevant concentration of 10 μg/L imidacloprid caused a reduction in bumblebee foraging activity, locomotion, and foraging rhythmicity, which could reduce foraging and pollination opportunities and reduce the ability of the colony to grow and reproduce.
24 citations
TL;DR: Field-relevant concentrations of imidacloprid, clothianidin and thiamethoxam disrupted learning, behavioural rhythmicity and sleep whilst thiacloprid exposure only affected sleep, demonstrating that neonicotinoid effects are likely mediated in the mushroom body and clock circuitry.
Abstract: Globally, neonicotinoids are still the most used insecticides, despite their well-documented sub-lethal effects on beneficial insects. Neonicotinoids are agonists at the nicotinic acetylcholine receptors, the main mediator of synaptic transmission in the insect brain, making them highly potent neurotoxins and insecticides. Memory, circadian rhythmicity and sleep are essential for efficient foraging in many pollinating insects, and involve nicotinic acetylcholine receptor signalling. The effect of field-relevant concentrations of European Union-banned neonicotinoids: imidacloprid, clothianidin and thiamethoxam, as well as the currently unbanned thiacloprid were tested on Drosophila memory, circadian rhythms and sleep. Field-relevant concentrations of imidacloprid, clothianidin and thiamethoxam disrupted learning, behavioural rhythmicity and sleep whilst thiacloprid exposure only affected sleep. Exposure to imidacloprid and clothianidin directly affected neurophysiology, preventing the day/night remodelling and accumulation of pigment dispersing factor neuropeptide in the dorsal terminals of clock neurons. Knockdown of the neonicotinoid susceptible Dα1 and Dβ2 nicotinic acetylcholine receptor subunits in the mushroom bodies or clock neurons recapitulated the neonicotinoid like deficits in memory or circadian/sleep behaviour demonstrating that neonicotinoid effects are likely mediated in the mushroom body and clock circuitry. Disruption to learning, circadian rhythmicity and sleep are likely to have far-reaching detrimental effects on beneficial insects in the field.
15 citations
TL;DR: The data show that the dysb1 mutant exhibits some behavioral deficits that mirror some aspects of the endophenotypes associated with the negative symptoms of schizophrenia, and argues that at least part of the behavioral aspects associated with these symptoms could be explained by a serotonergic deficit.
11 citations
TL;DR: It is shown that exposure to the field relevant concentration of 10 µg/L of imidacloprid can cause a reduction in foraging activity and reduce both locomotor and foraging rhythmicity in Bombus terrestris.
Abstract: Neonicotinoids have been implicated in the large declines observed in flying insects such as bumblebees, an important group of pollinators. Neonicotinoids are agonists of nicotinic acetylcholine receptors that are found throughout the insect central nervous system, and are the main mediators of synaptic neurotransmission. These receptors are important for the function of the insect central clock and circadian rhythms. The clock allows pollinators to coincide their activity with the availability of floral resources, favourable flight temperatures, as well as impacting learning, navigation and communication. Here we show that exposure to the field relevant concentration of 10 μg/L of imidacloprid can cause a reduction in foraging activity and reduce both locomotor and foraging rhythmicity in Bombus terrestris. Foragers showed an increase in daytime sleep and an increase in the proportion of activity occurring at night. This would likely negatively impact foraging and pollination opportunities, reducing the ability of the colony to grow and reproduce, endangering crop yields.
1 citations
TL;DR: The results support a conserved relationship between enhanced BK channel function and disrupted motor control across distantly related species.
Abstract: Background Genetic and in vitro studies have linked a heterozygous gain-of-function mutation (D434G) in the hSlo1 BK (Big potassium) channel to paroxysmal dyskinesia. However, support for this linkage from in vivo models has been lacking. Objectives We aimed to re-create the equivalent mutation to hSlo1 D434G in the fruit fly, Drosophila, and examine how this mutation altered movement and action potential waveforms. Methods We generated a knock-in Drosophila model of hSlo1 D434G. We used video-tracking and infra-red beam-break systems to test whether locomotion was altered in this model, and patch-clamp electrophysiology to determine how the mutation affected action potential waveforms. Results We identified profound motor dysfunction and sporadic leg twitches, as well as a reduced width and an enhancement of the afterhyperpolarization phase of action potentials, in the model background. Conclusion Our results support a conserved relationship between enhanced BK channel function and disrupted motor control across distantly related species.
1 citations