Effects of subchronic aluminum lactate exposure on learning and memory and transportation of Aβ in blood-cerebrospinal fluid in rats

Abstract

To investigate the effects of aluminum lactate exposure on learning and memory and the transportation of amyloid-beta peptides(Aβ) in cerebrospinal fluid in rats. A total of 80 male Sprague-Dawley rats were randomly divided into solvent control(distilled water) group and low-, medium-, and high-dose aluminum poisoning groups(10, 30, and 90 mg/kg aluminum lactate), with 20 rats in each group, and the poisoning procedure was performed by gavage for 2 months. The Morris water maze test was used to test the rats' learning and memory, Western blot was used to measure the expression level of low-density lipoprotein receptor protein-1(LRP-1) in rats' choroid plexus, and enzyme-linked immunosorbent assay(ELISA) was used to measure the content of Aβ in the cerebrospinal fluid and plasma. The Morris water maze test showed that in the place navigation test, with the increasing training time, the escape latency was significantly shortened in each group and showed significant differences between any two groups(P<0.05). In the spatial probe test, the time spent in target quadrant in the medium-and high-dose groups was 11.52±1.56 s and 10.43±5.27 s, respectively, which was significantly shorter than that in the control group and the low-dose group(15.81±3.01 s and 13.91±2.17 s)(P<0.05). The numbers of platform crossings in the medium-and high-dose groups were 2.64±1.39 and 1.50±0.76, respectively, which were significantly lower than those in the control group and the low-dose group(4.29±0.914 and 3.56±1.38)(P<0.05). The results of ELISA showed that the medium-and high-dose groups had significant increases in the content of Aβ1-42 in cerebrospinal fluid(320.35±84.82 pg/ml and 327.68±67.51 pg/ml), which was significantly higher than that in the control group(203.46±74.36 pg/ml) (P<0.05). The content of Aβ1-42 in plasma showed no significant difference between any two groups(P>0.05), and that of Aβ1-40 in cerebrospinal fluid and plasma also showed no significant difference between any two groups(P>0.05). The results of Western blot showed that the high-dose group had significantly lower protein expression of LRP-1 than the control group and the low-and medium-dose groups(0.57±0.21 vs 1.00±0.00/0.79±0.15/0.95±0.24, P<0.05). Subchronic aluminum exposure may reduce learning and memory in rats, and the accumulation of Aβ in cerebrospinal fluid may be related to the reduced protein expression of LRP-1 in the choroid plexus, suggesting that aluminum affects learning and memory in rats through reducing the protein expression of LRP-1, influencing the transportation of Aβ, and leading to the accumulation of Aβ.