Meeting Abstract
Neonicotinoid insecticides are used extensively in agriculture in North America, despite known environmental impacts. These insecticides affect foraging behaviour and navigation in non-target insects, although the mechanisms of these effects are not fully understood. A visual motion sensitive neuron in the locust (Locusta migratoria), the Descending Contralateral Movement Detector (DCMD), integrates visual information and is involved in eliciting escape behaviours. The DCMD receives coded input from the compound eyes and synapses with motorneurons involved in flight and jumping. We show that imidacloprid (IMD), a neonicotinoid insecticide, impairs neural and behavioural responses to visual stimuli at sublethal concentrations, and these effects are sustained two and twenty-four hours after treatment. Exposure to 10 ng/g IMD (ng IMD per g locust body weight) attenuates escape manoeuvers while 100 ng/g IMD inhibits the ability to fly and walk. Behavioural effects correlated with attenuated neural responses: IMD disrupted DCMD bursting, a coding property important for motion detection. Specifically, IMD reduced the DCMD peak firing rate within bursts at ecologically relevant doses of 10 ng/g. Thus, IMD causes significant and lasting impairment of an important pathway involved with visual sensory coding and escape behaviours at ecologically-relevant doses. These results show, for the first time, that a neonicotinoid insecticide directly impairs an important, taxonomically conserved motion-sensitive visual network.
