34Inhibition of acetylcholinesterase by either organophosphates or carbamates causes anti-35 cholinesterase poisoning. This arises through a wide range of neurotoxic effects triggered by the 36 overstimulation of the cholinergic receptors at synapses and neuromuscular junctions. Without 37 intervention, this poisoning can lead to profound toxic effects, including death, and the incomplete 38 efficacy of the current treatments, particularly for oxime-insensitive agents, provokes the need to find 39 better antidotes. Here we show how the non-parasitic nematode Caenorhabditis elegans offers an 40 excellent tool for investigating the acetylcholinesterase intoxication. The C. elegans neuromuscular 41 junctions show a high degree of molecular and functional conservation with the cholinergic 42 transmission that operates in the autonomic, central and neuromuscular synapses in mammals. In fact, 43 the anti-cholinesterase intoxication of the worm's body wall neuromuscular junction has been 44 unprecedented in understanding molecular determinants of cholinergic function in nematodes and 45 other organisms. We extend the use of the model organism's feeding behaviour as a tool to investigate 46 carbamate and organophosphate mode of action. We show that inhibition of the cholinergic-47 dependent rhythmic pumping of the pharyngeal muscle correlates with the inhibition of the 48 acetylcholinesterase activity caused by aldicarb, paraoxons and DFP exposure. Further, this bio-assay 49 allows one to address oxime dependent reversal of cholinesterase inhibition in the context of whole 50 organism recovery. Interestingly, the recovery of the pharyngeal function after such anti-51 cholinesterase poisoning represents a sensitive and easily quantifiable phenotype that is indicative of 52 the spontaneous recovery or irreversible modification of the worm acetylcholinesterase after 53 inhibition. These observations highlight the pharynx of C. elegans as a new tractable approach to 54 explore anti-cholinesterase intoxication and recovery with the potential to resolve critical genetic 55