Figure 2: Cholinergic pesticides depolarize KCs at low concentrations.
From: Cholinergic pesticides cause mushroom body neuronal inactivation in honeybees
The effect of neonicotinoids and coumaphos oxon on KC membrane potential (VM) and AP firing were investigated under current clamp. (a) Bath application of clothianidin evokes sustained depolarization of KC VM. Coapplication of the nAChR antagonist d-TC (500 μM, here and subsequently) reverses the depolarization, indicating that it is mediated by nAChR activation. (b) AP firing is transiently observed during the development of the depolarization (2 min after clothianidin application), but is inhibited during the subsequent sustained depolarization (20 min example trace). (c) Coumaphos oxon evokes a more slowly developing depolarization of KC VM, which is reversed by d-TC. The slower time course is consistent with nAChR activation by accumulated ACh as a result of AChE inhibition. (d) AP firing is again transiently observed during the development of the depolarization (15 min after coumaphos oxon application) but not during the sustained phase (30 min example trace). (e) Dose dependence of the mean (±s.e.m.) depolarizing effects of the neonicotinoids clothianidin (black square, n=4) and imidacloprid (black circle, n=3-4), the metabolite imidacloprid–olefin (open circle, n=4) and the organophosphate coumaphos oxon (grey triangle, n=2–7; n numbers refer to each data point; for all data points ≥10 nM, P<0.05, paired t-test). (f) Mean (±s.e.m.) data showing the reversal by d-TC of the depolarizations evoked by clothianidin (10–100 nM, n=3), imidacloprid (50–500 nM, n=4), imidacloprid–olefin (500 nM, n=3) and coumaphos oxon (200 nM–1 μM, n=4). All four pesticides potently modulate KC excitability by causing sustained activation of nAChRs.
