Cognitive impairment in rats induced by nano-CuO and its possible mechanisms.

Abstract Several studies have reported the adverse effects of nano-CuO on hippocampal CA1 neuron, whereas little has been known about nano-CuO neurotoxicity in vivo. In the present study, we investigated the effects of nano-CuO on spatial cognition and electrophysiological alterations in rats. In addition, histological and biochemical changes in rat's hippocampus were measured as well. Morris water maze (MWM) test showed that learning and memory abilities in nano-CuO-treated group were weakened significantly. The long-term potentiation (LTP) test exhibited that field excitatory postsynaptic potentials (fEPSPs) slopes were significantly lower in nano-CuO-treated group compared to that in control group. Furthermore, the levels of ROS and malonaldehyde (MDA) in hippocampal homogenate of nano-CuO-treated group were considerably enhanced while the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were statistically reduced. Moreover, the enhanced 4-hydroxynonenal (HNE) and caspase-3 implied the progression of apoptosis in the hippocampus. The results suggested that the neuronal damage, induced by impairing oxidation–antioxidation homeostasis, led to the impairment of hippocampal LTP, which was associated with the poor performance of animals in behavior tests.