Highlights
Acute exposure to phthalates affects fundamental aspects of adult brain function.
The effects are massive both with DEHP and its substitute DINP.
Both plasticizers affect neuronal signaling and central information processing.
Both offset the balance between excitation and inhibition.
Both cause a massive decline in conduction speed and potentially impact neuroglia.
Abstract
Phthalates are key additives in many plastic products and among the most frequently used plasticizers. The release of some of them into the environment has been shown to have serious effects on development and reproduction. Based on such effects, diisononyl phthalate (DINP) has been advocated as a safer alternative to di-2-ethylhexyl phthalate (DEHP). Recently, it has been suggested that DEHP may affect the vertebrate blood-brain barrier. This could have serious consequences not only for the developing, but also for the adult brain. Here we tested for such impact on neuronal function and demonstrate acute exposure effects of both plasticizers on fundamental aspects of brain function in an adult vertebrate. We used the Mauthner neuron in the hindbrain of fish and its diverse inputs from various sensory systems as a model. After exposing intact goldfish to environmentally relevant plasticizer concentration (either 100 µg L–1, or 10 µg L–1), we show from in vivo intracellular recording that one month of environmental exposure to DEHP or DINP affected the sensory input to this central neuron, offset the balance between excitation and inhibition, and reduced its conduction speed by 20 %. The effects of both plasticizers were strong even at the concentration of 10 µg L–1. In an adult vertebrate, our findings thus demonstrate a previously neglected high sensitivity of various crucial brain functions to the acute exposure to phthalates.