铝暴露对大鼠海马神经元长时程增强和Na+通道表达的影响

海马神经元长时程增强(LTP) 被认为与学习和记忆的形成有关.Na⁺在诱导 LTP产生的过程中十分重要.实验发现，慢性铝暴露可以影响大鼠海马神经元LTP的产生，随着铝暴露浓度的增加，LTP 的幅值逐渐降低.RT-PCR 法对大鼠海马神经元 9 种类型Na⁺ 通道（即 Nav1.1～Nav1.9）的 mRNA 进行检测发现,除 Nav1.4 和 Nav1.8 Na⁺通道 mRNA 在大鼠海马神经元中未见表达外，慢性染铝组大鼠海马神经元7种Na⁺ 通道 mRNA 表达均明显增高（P<0.05）.蛋白印迹法对一种脑型 Na⁺通道 (Nav 1.2) 蛋白检测证明, Na⁺通道蛋白表达亦明显升高.结果提示，铝进入神经元后，可能通过影响 Na⁺ 通道蛋白的表达而影响了突触后神经细胞的去极化，进而影响了LTP的诱导过程，从而预示铝的暴露可能损害大鼠学习和记忆能力.

Aluminum Exposure Alters Long-term Potentiation and Expressions of Sodium Channels in Hippocampus

Long-term potentiation (LTP) is a sustainable increase in the postsynaptic potential due to the rapidly repetitive stimulation applied in presynaptic neurons in a short period of time, which is considered as the basis for learning and memory formation. Sodium is one of the most important ions in the process of LTP induction, as the sodium influx causes a depolarization called the excitatory postsynaptic potential (EPSP). The high frequency stimuli causes the progressive depolarization of neurons as a result of EPSP summation, which relieves the magnesium blocked of the NMDA receptor, promotes the calcium influx and triggers the formation of LTP. Chronic aluminum exposure was reported to inhibit LTP induction and cut down LTP amplitude.The mRNA levels of 9 types of sodium channels, including Nav1.1-Nav1.9, have been analyzed by semi-quantitative RT-PCR from the rat hippocampal neurons.The results showed that 7 of the sodium channels were significantly increased (P<0.05) at mRNA levels following chronic aluminum exposure, except for Nav1.4 and Nav1.8. The protein expression of Nav 1.2(the brain-type sodium channel) was significantly increased by Western blot analysis. It was concluded that chronic aluminum exposure might impair the learning and memory function by altering the expressin of sodium channels, therefore, affecting the postsynaptic depolarization required for the induction of LTP.