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Lanthanum (La) accumulates resulted in detrimental alterations in the morphology and structure of hippocampal neurons, but the specific mechanism remains unclear. At 49 days after the birth of LaCl 3 -exposed offspring rats, number of Nissl bodies and the neural cell structure in hippocampal tissue was evaluated by Nissl and HE staining; the ultrastructure of hippocampal CA1 zone was observed by electron microscopy. Learning and memory ability of the offspring decreased after LaCl 3  exposure. Nissl staining showed that in the La-exposed rats, Nissl body number in the hippocampus was significantly decreased, and the cell arrangement was disordered. The ultramicroscopic structure of hippocampal neurons in La-exposed rats showed that the mitochondrial volume was increased; ridges were shorter, decreased in number, and marginally shifted; and the matrix electron density was also decreased. The contents of TNFR1, P-RIPK1, P-RIPK3, and P-MLKL in hippocampal neurons increased significantly as the LaCl 3  dose increased. La exposure retarded the growth and development of offspring rat, resulted hippocampal nerve cell necroptosis, and impaired spatial learning and memory, which related to abnormal expression of TNFR-RIPK1/RIPK3 pathway.

The TNFR-RIPK1/RIPK3 signalling pathway mediates the effect of lanthanum on necroptosis of nerve cells