Study on neonatal neurons and learning and memory in A53T-α-synucleintransgenic mice

Objective To investigate the effect of α-synucleinmutation on learning and memory in A53T-α-synuclein transgenic mice and related mechanisms. Methods A53T-α-synuclein transgenic mice with positive gene identification were selected as an experimental group, while those with the same gender and negative identification were used as a control group. The spatial memory capacity of mice was detected by Y-maze test.5-Bromodeoxyuridine (BrdU) anddoublecortin (DCX) fluorescence staining were used to detect the number of newborn neurons in the dentate gyrus (DG) area. The morphology of hippocampal pyramidal cells was observed by Golgi staining, and the level of Fos protein in the hippocampus was detected by immunofluorescence. Results Compared with the control group, the number of A53T-α-synuclein transgenic mice entering into the Y-maze novel arm, retention time and activity distance were remarkably reduced (P< 0.05);the number of BrdU and DCX positive cells in DG area was decreased (P< 0.05);pyramidal cell body was shrunk, dendritic branch and length and the density of dendritic spines were reduced (P< 0.05);and level of Fos protein in the hippocampus was declined (P< 0.05). Conclusions The missense mutation of α-synuclein can inhibit neurogenesis in the hippocampus, reduce the plasticity of hippocampal synapses, and induce the down-regulation of Fos protein expression, which leads to impaired spatial memory capacity in mice.