Studies have reported that lanthanum chloride (LaCl₃) can across the blood-brain barrier, accumulate in the brain and affect the spatial learning and memory abilities. However, the potential mechanism that LaCl₃-induced neurotoxic effects has not yet been defined. Glutamate (Glu) is a vital excitatory neurotransmitter, and the excessive Glu accumulation in extracellular space can induce excitatory neurotoxicity. This study was designed to research the influence of LaCl₃ on the spatial learning and memory abilities of rats and to discuss the possible mechanism underlying this effect regarding the extracellular Glu concentration, the Glu-glutamine (Gln) cycle and the N-methyl-D-aspartate (NMDA) receptors. Four groups of Wistar rats were exposed to 0%, 0.125%, 0.25% or 0.5% LaCl₃ via the drinking water from the day of conception to 1 month after weaning. These results showed that LaCl₃ exposure damaged spatial learning and memory, long-term potentiation, and neuronal ultrastructure, generated an excessive accumulation of glutamate, significantly decreased the expression of glutamate/aspartate transporter (GLAST), glutamate transporter-1 (GLT-1), glutamine synthetase (GS) and phosphate-activated glutaminase (PAG), and increased the expression of GluN1, GluN2A and GluN2B. This study showed that LaCl₃ impaired the rats' spatial learning and memory abilities by disturbing the Glu-Gln cycle and over-activating NMDA receptors thereby inducing excitotoxicity.

研究报告说，氯化镧（LaCl ₃）可以穿过血脑屏障，在大脑中蓄积并影响空间学习和记忆能力。但是，尚未确定LaCl ₃诱导的神经毒性作用的潜在机制。谷氨酸（Glu）是一种重要的兴奋性神经递质，细胞外空间中过多的Glu积累会诱发兴奋性神经毒性。本研究旨在研究LaCl ₃的影响关于大鼠的空间学习和记忆能力，并探讨有关这种作用的可能机制，涉及细胞外Glu浓度，Glu-谷氨酰胺（Gln）循环和N-甲基-D-天冬氨酸（NMDA）受体。从受孕日到断奶后1个月，四组Wistar大鼠通过饮用水分别接触0％，0.125％，0.25％或0.5％LaCl ₃。这些结果表明，LaCl ₃暴露破坏空间学习和记忆，长期增强和神经元超微结构，产生过量的谷氨酸积累，显着降低谷氨酸/天冬氨酸转运蛋白（GLAST），谷氨酸转运蛋白-1（GLT-1），谷氨酰胺合成酶（GS）的表达）和磷酸激活的谷氨酰胺酶（PAG），并增加了GluN1，GluN2A和GluN2B的表达。这项研究表明，LaCl _3会干扰Glu-Gln循环并过度激活NMDA受体，从而引起兴奋性中毒，从而损害大鼠的空间学习和记忆能力。