The central nervous system (CNS) toxicity induced by exposure to nano-sized particles is of great concern, but the mechanism of how this toxicity may be incurred has yet to be elucidated. Here, we examined how N-methyl-D-aspartate (NMDA) receptor-mediated postsynaptic signalling cascade may be affected by titanium dioxide particles (TiO 2 NPs) exposure for six consecutive months to contribute to the observed neurotoxicity. The results suggest that long-term exposure to TiO 2 NPs led to titanium

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... accumulation and iron reduction in the blood and hippocampus tissues, and significant hippocampal injury as well as reduction of learning and memory in mice. The CNS injuries following longterm TiO 2 NP exposure were closely associated with significant reductions in NR1, NR2A, NR2B, calcium/calmodulindependent protein kinase II, postsynaptic density protein 95, nuclear activated extracellular-signal regulated kinase (ERK1/2), Dexras1, CAPON, peripheral benzodiazepine receptor-associated protein, and divalent metal transporter as well as elevation of synaptic Ras GTPase-activating protein and neural nitric oxide synthase in the hippocampus. It implies that long-term exposure to TiO 2 NPs may induce neurotoxic effects via impairing NMDA receptor-mediated postsynaptic signalling cascade in animals. connecting NMDARs to divergent signal transduction pathways [26] . Its overexpression can inhibit LTP and decrease LTD induction Journal of Nanomedicine & Nanotechnology J o u rna l of N a n o m ed icine & N a n o te chnolo g y