A central question is whether potassium (K+) channels, which are key regulators of neuronal excitability, are targets of reactive oxygen species (ROS) and whether these interactions have a role in the mechanisms underlying neurodegeneration. Here, we show that oxidation of K+ channel KVS-1 during ageing causes sensory function loss in Caenorhabditis elegans, and that protection of this channel from oxidation preserves neuronal function. Chemotaxis, a function controlled by KVS-1, was significantly impaired in worms exposed to oxidizing agents, but only moderately affected in worms harboring an oxidation-resistant KVS-1 mutant (C113S). In ageing C113S transgenic worms, the effects of free radical accumulation were significantly attenuated compared to wild type. Electrophysiological analyses showed that both ROS accumulation during ageing, or acute exposure to oxidizing agents, acted primarily to alter the excitability of the neurons that mediate chemotaxis. Together, these findings establish a pivotal role for ROS-mediated oxidation of voltage-gated K+ channels in sensorial decline during ageing in invertebrates.