Aluminum exposure has been reported to be related to learning and memory impairment. This study examines the role of aluminum in alterating amino acids of the cerebral cortex of rats. The Step-down type tests were performed to investigate the alteration of learning and memory of rats induced by aluminum. The amino acids in the cerebral cortex were detected by high performance liquid chromatography (HLPC). Results show that the amounts of aluminum in the cerebral cortex increased by 5.0mgAl3+/(Kg·BW) group and 10.0mg Al3+/(Kg·BW) group. In the Step-down type test, the EN1 increased significantly in the Al3+ 10.0mg/(Kg·BW) group. The latency shortened obviously and the EN2 increased significantly in the 10.0mg Al3+/(Kg·BW) group. The content of Glu (Glutamic acid) increased but the content of GABA (gamma-aminobutyric acid) decreased significantly in the 10.0mg Al3+/(Kg·BW) group. This present study shows evidence that the disorder of amino acid neurotransmitters system plays an important role in the impairment of learning and memory of rats induced by aluminum.
<b><i>Introduction:</i></b> Substantial evidence has indicated that isoflurane leads to learning and memory impairment. This study was designed to investigate the potential role of microRNA-124-3p (miR-124-3p) in isoflurane-induced learning and memory impairment in rats. <b><i>Methods:</i></b> Spatial learning and memory of rats were estimated by the Morris water maze (MWM) test after the construction of isoflurane-treated models. qRT-PCR was performed to assess the expression levels of miR-124-3p. The levels of interleukin-1β, interleukin-6, and tumor necrosis factor-α in the hippocampal tissues were determined by enzyme-linked immunosorbent assay. The luciferase activity was determined by using a dual-luciferase reporter assay system. <b><i>Results:</i></b> The higher escape latency and lower time spent in the original quadrant were shown in isoflurane-treated rats compared with the control rats. Moreover, treatment with isoflurane could induce neuroinflammation, and miR-124-3p was poorly expressed in the hippocampal tissue of isoflurane-treated rats. Furthermore, STAT3 is a functional target of miR-124-3p, and inflammatory cytokine level was downregulated by miR-124-3p. <b><i>Discussion/Conclusion:</i></b> Combining the results of the current study demonstrates that miR-124-3p may have pivotal roles in improving isoflurane-induced learning and memory impairment via targeting STAT3 and inhibiting neuroinflammation.
Role of Endoplasmic Reticulum Stress in Learning and Memory Impairment and Alzheimer's Disease-Like Neuropathology in the PS19 and APPSwe Mouse Models of Tauopathy and Amyloidosis