Acute β-tetrabromoethylcyclohexane (β-TBECH) treatment inhibits the electrical activity of rat Purkinje neurons

Brominated flame-retardants are environmentally pervasive and persistent synthetic chemicals, some of which have been demonstrated to disrupt neuroendocrine signaling and electrical activity of neurons. 1,2-dibromo-4-(1,2-dibromoethyl)-cyclohexane (TBECH) lacks the toxicity of other classes of BFRs, however its safety is still questioned, as little is known of its neurological effects. Therefore, we sought to determine if TBECH could acutely alter the electrical activity of Purkinje neurons maintained in vitro. Briefly, cerebella from gestational day 20 rats were dissociated and maintained for up to three weeks in culture. Action potentials of Purkinje neurons were detected by cell-attached patch clamp before, during, and after application of beta-TBECH. beta-TBECH decreased action potential activity in a dose-dependent manner with an apparent EC50 of 396 nM. beta-TBECH did not significantly alter the coefficient of variation, a measure of the regularity of firing, suggesting that the mechanism of beta-TBECH's effects on firing frequency may be independent of Purkinje neuron intracellular calcium handling. Because levels of beta-TBECH in exposed individuals may not approach the EC50, these data suggest that any abnormal neu-rodevelopment or behavior linked with beta-TBECH exposure may result from endocrinological effects as opposed to direct disruption of electrical activity. (C) 2019 Elsevier Ltd. All rights reserved.