Effect of Acetamiprid on spatial memory and hippocampal glutamatergic system

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Abstract
Acetamiprid (ACE) is one of the widely used neonicotinoid insecticides. In mammals, in spite of the low-affinity nAChRs, neurotoxic effects following the Acetamiprid exposure have recently been reported, which suggests some concerns regarding the impacts on the nervous system of mammals. This study aims to investigate the effect of Acetamiprid on spatial memory and possible vulnerability of hippocampal glutamatergic system following the Acetamiprid exposure. 10, 20, and 40 mg/kg doses of Acetamiprid were administered to male rats by gavage once per day for 28 days. The spatial memory was examined with the Morris water maze apparatus. The amount of Acetamiprid in the serum and hippocampus was measured. In addition, glutamate level and changes in the expression of NR1, NR2, and NR2B genes were measured in the hippocampus; also, the hippocampus tissue was histologically evaluated. A significant increase in training parameters which consist of escape latency and traveled distance was observed on the first and second day of training in Acetamiprid-treated groups (20 and 40 mg/kg) compared to the control group (p < 0.001). In the probe test, rats in all Acetamiprid-treated groups significantly spent less time in the target quadrant compared to the control group (p < 0.001). Acetamiprid concentration dose dependently increased in the serum and in the hippocampus followed by Acetamiprid exposure. In all Acetamiprid-treated groups, a significant reduction of glutamate level in the hippocampus was observed (p < 0.05). The reduction of NR1, NR2A, and NR2B gene expression in the hippocampus was observed at a dose of 20 mg/kg. The histological evaluation showed neural degeneration in the dentate gyrus area of the hippocampus at a dose of 40 mg/kg in the Acetamiprid-treated group. The results of the present study indicate that Acetamiprid impairs memory consolidation through the reduction of glutamate and the expression of NMDA receptor subunits in the hippocampus at low doses, along with the loss of neural cells in dentate gyrus at high dose.

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