Abstract
Triclosan, a widely used industrial and household agent, is present as an antiseptic ingredient in numerous products of everyday use, such as toothpaste, cosmetics, kitchenware, and toys. Previous studies have shown that human brain and animal tissues contain triclosan, which has been found also as a contaminant of water and soil. Triclosan disrupts heart and skeletal muscle Ca2+ signaling, damages liver function, alters gut microbiota, causes colonic inflammation, and promotes apoptosis in cultured neocortical neurons and neural stem cells. Information, however, on the possible effects of triclosan on the function of the hippocampus, a key brain region for spatial learning and memory, is lacking. Here, we report that triclosan addition at low concentrations to hippocampal slices from male rats inhibited long-term potentiation but did not affect basal synaptic transmission or paired-pulse facilitation and modified the content or phosphorylation levels of synaptic plasticity-related proteins. Additionally, incubation of primary hippocampal cultures with triclosan prevented both the dendritic spine remodeling induced by brain-derived neurotrophic factor and the emergence of spontaneous oscillatory Ca2+ signals. Furthermore, intra-hippocampal injection of triclosan significantly disrupted rat navigation in the Oasis maze spatial memory task, an indication that triclosan impairs hippocampus-dependent spatial memory performance. Based on these combined results, we conclude that triclosan exerts highly damaging effects on hippocampal neuronal function in vitro and impairs spatial memory processes in vivo.
Highlights
The production and utilization of chemical agents designed to reduce household and human bacterial load is currently on the rise (Levy, 2001; Aiello and Larson, 2003; Dhillon et al, 2015)
In agreement with the LTP and structural plasticity impairments caused by TCS, we found that after three intra-hippocampal TCS injections, which presumably yielded a final hippocampal TCS concentration of up to ∼18 nM, rats displayed significant defects in the performance of a spatial memory task
Addition of up to 10 μM TCS to RyR channels from brain cortex incorporated in planar lipid bilayers does not affect RyR single channel properties (Bull et al, manuscript in preparation). Based on these combined results, we suggest that TCS disturbs Ca2+ entry pathways required for neuronal calcium-dependent responses, including CamKII-α phosphorylation, LTP, dendritic spine remodeling, and hippocampus-dependent spatial memory
Summary
The production and utilization of chemical agents designed to reduce household and human bacterial load is currently on the rise (Levy, 2001; Aiello and Larson, 2003; Dhillon et al, 2015). Triclosan induces Fasdependent apoptosis in neocortical neurons in vitro (Szychowski et al, 2015) and produces toxic effects in neural stem cells through mechanisms involving increased reactive oxygen species (ROS) production and apoptosis (Park et al, 2016), leading to the proposal that TCS acts as a neurotoxic agent (Ruszkiewicz et al, 2017). In consonance with this idea, incubation of primary neocortical neurons with TCS decreases the expression of N-methyl-D-aspartate (NMDA) receptor (NMDAR) subunits and enhances NMDAR-dependent ROS generation and caspase-3-dependent apoptosis (Szychowski et al, 2018). If chronic TCS exposure were to produce these damaging effects in the human brain, the presence of TCS in personal care products should be reconsidered
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