Effect of Lanthanum on Synaptic Plasticity in Hippocampus of Offspring Rats

Abstract

In view of the effect of Lanthanum (La) on synaptic plasticity in offspring rats and its mechanism, 32 pregnant adult Wistar rats were divided into four groups randomly: control group (NC), 0.25%, 0.5% and 1.0% LaCl3 groups (n=8). All rats were poisoned through free drinking from day 0 of pregnancy to postnatal pregnancy to postnatal day 21 (suckling period). Morris was used to observe the spatial learning and memory ability of the offspring. The ultrastructure of hippocampus was observed by electron microscope. Expressions of synapsin, SYN, PSD95, NMDAR1, SHANK1, SHANK3 and GluR2 in the hippocampus were tested by qPCR and Western blot. The distribution and expression of functional synapses NMDAR1-SYN and PSD95 in CA1, CA3 and DG regions of hippocampus were analyzed by immunofluorescence. With increasing LaCl3 dose, the learning and memory abilities of offspring rats were significantly declined than those of NC group. Compared with NC group, there were abnormal changes in the ultrastructure of hippocampal tissue in LaCl3 groups, such as the shortening of synaptic active band, the thinning of postsynaptic density, and the decreasing of curvature of synaptic interface. The most obvious abnormal changes were found in the 1.0% LaCl3 group. The expressions of both mRNA and proteins (synapsin, SYN, PSD-95, NMDAR, SHANK1, SHANK3 and GluR2) in the hippocampus of the LaCl3 groups were significantly lower than those of NC group, and decreased with increasing LaCl3 dose. Compared with the control group, the co-expression of NMDAR1-SYN and the expression of PSD95 in CA1, CA3 and DG of hippocampus decreased significantly with the increase of Lanthanum exposure dose. Collectively, the mechanism of the decrease of learning and memory ability in offspring rats may be closely related to the abnormal expression of synaptic plasticity related proteins and the effect of Lanthanum exposure on synaptic transmission.