Kava is a tranquilizing beverage from the South Pacific Islands that contains lipophilic compounds called kavalactones. Ingestion of these compounds is known to produce sedative and anxiolytic effects; however, the mechanisms underlying these changes are not fully elucidated. Previously, we have shown that administration of kavalactones enhanced neuromuscular excitation in C. elegans nematodes, demonstrated by epileptic-like convulsions and paralysis in a dose-responsive manner. This response suggests an increase in acetylcholine (ACh) transmission at the neuromuscular junction (NMJ). Based on the nature of lactones, we hypothesized that kavalactones may mediate ACh transmission through the inhibition of acetylcholinesterase (AChE) enzyme. We tested this hypothesis by evaluating the responses of C. elegans worms harboring loss-of-function mutations in certain AChE genes. Our results showed that AChE loss-of-function mutants displayed hypersensitivity to kavalactones. In concert, the same mutants displayed hypersensitivity to aldicarb, a known AChE inhibitor. These results suggest that kavalactones may impact ACh signaling via AChE.

Effects of kavalactones on acetylcholinesterase (AChE) activity in Caenorhabditis elegans

2019 Spring National Meeting

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