Effects of Chronic Aluminum Lactate Exposure on Neuronal Apoptosis and Hippocampal Synaptic Plasticity in Rats.

Abstract

This study investigated the effects of chronic aluminum exposure on apoptosis of hippocampal neurons, and synaptic plasticity in the hippocampus in rats. Rats were divided into the control, low-dose (L-Al), mid-dose (M-Al), and high-dose (H-Al) groups. After chronic exposure of aluminum, the Morris water maze (MWM) and open-field (OF) tests were performed to assess the behavioral performance. Electrophysiological measurements were conducted. Flow cytometry was used to assess the apoptotic processes. Quantitative real-time PCR and ELISA were performed to measure mRNA and protein expression levels of caspases. After 90days of aluminum exposure, the aluminum contents in the brain of the rats were increased, with the increasing exposure dose. The MWM and OF tests showed that chronic exposure of aluminum significantly impaired the neurobehavior of rats. Moreover, after high-frequency stimulation (HFS), the average amplitudes of field excitatory postsynaptic potentials (fEPSPs) for the M-Al and H-Al groups were lower than the control group at 10, 20, 30, 40, 50, and 60min. Furthermore, the apoptotic rates in the M-Al and H-Al groups were significantly higher than the control group. The qRT-PCR and ELISA showed that, compared with the control group, the mRNA and protein expression levels of caspases-3, -8, and -9 were significantly increased in the aluminum-treated groups compared with the control group. Long-term exposure to aluminum could induce the apoptosis of hippocampal neurons, damage the synaptic plasticity, and impair the learning and memory functions in rats. There might be a close relationship between the neuronal apoptosis and synaptic plasticity damage.