Nicotine induces abnormal motor coupling through sensitization of a mechanosensory circuit in Caenorhabditis elegans.

ABSTRACT: Nicotine exposure elicits diverse behavioral changes, yet the underlying neural pathways and molecular mechanisms remain incompletely understood. Here, we demonstrate that chronic nicotine exposure markedly increases both the initiation and duration of reversals in Caenorhabditis elegans. Strikingly, these reversals were tightly coupled with the rhythmic body contractions of the defecation motor program (DMP). Through pharmacological, genetic, in situ electrophysiological, and calcium imaging analyses, we show that nicotine enhances the activity of the AVA interneuron via selective upregulation of ACR-16, a nicotinic ACh receptor critical for nicotine-induced motor coupling. Ablation of touch receptor neurons (TRNs) or inhibition of TRNs-mediated mechanosensation completely abolished this

SUBMITTER: Liu Y 

PROVIDER: S-EPMC12507281 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature