Abnormal visual processing and increased seizure susceptibility result from developmental exposure to the biocide methylisothiazolinone.

Methylisothiazolinone (MIT) is a commonly used biocide known to be neurotoxic in vitro. Brief exposure of cortical neurons in culture to MIT results in increased neurodegeneration, whereas chronic exposure of developing neurons in culture to low concentrations of MIT has been shown to interfere with normal neurite outgrowth. However, the effects of chronic MIT exposure on the developing nervous system have not been tested in vivo. Here we expose Xenopus laevis tadpoles to sub-lethal concentrations of MIT during a critical period in neural development. We find that MIT exposure results in deficits in visually mediated avoidance behavior and increased susceptibility to seizures, as well electrophysiological abnormalities in optic tectal function, without any effects on overall morphology, gross anatomy of the visual projections, overall visual function, and swimming ability. These effects indicate that chronic exposure to low levels of MIT results in neural circuit-level deficits that result in abnormal neurological function without causing increased mortality or even gross anatomical defects. Our findings, combined with the fact that the long-term neurological impacts of environmental exposure to MIT have not been determined, suggest a need for a closer evaluation of the safety of MIT in commercial and industrial products.