Objective To study the effect of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor palmitoylation modification on long-term potentiation in rat hippocampus by subchronic exposure to aluminum.
Methods Twenty-four healthy adult male SD rats were randomly divided by weight into control group, low-dose group, middledose group, and high-dose group, and administered with saline (control group) or Al(mal)3 (10, 20, and 40μmol/kg) via intraperitoneal injection every two days for 12 weeks. Field excitatory post-synaptic potentials in CA1 region were recorded by field LTP record technique in vivo, and AMPA receptor palmitoylation was examined by acyl-biotin exchange method.
Results The results of LTP record showed that the standardized amplitude (hereinafter referred to as "amplitude") of each group was significantly different at 1 min and 60 min after high frequency stimulation (P < 0.05), but not at 30 min. The amplitudes of the middle-and high-dose groups were statistically lower than those of the control group and the low dose group at 1min (P < 0.05). The amplitudes of the three dose groups were significantly lower than that of the control group at 60 min, and the amplitude of the high-dose group was significantly lower than those of the low-and middle-dose groups at 60 min (P < 0.05). The results of acyl-biotin exchange showed that the glutamate receptor 1 (GluR1) palmitoylation levels of the middle-and high-dose groups were statistically lower than that of the control group (P < 0.05); the glutamate receptor 2 (GluR2) palmitoylation level in the middle-dose group was statistically lower than that of the control group, and the GluR2 palmitoylation level in the high-dose group was statistically lower than those of the control, low-dose, and middle-dose groups (P < 0.05).
Conclusion Long-term potentiation in rat hippocampus is inhibited and palmitoylation of AMPA receptor is reduced after subchronic aluminum exposure, suggesting that the reduction of palmitoylation of AMPA receptor may be one of the mechanisms of LTP damage.
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