Abstract: Objective： To demonstrate the changes in the expression of NT3 and trkC in the hippocampal neurons of Alzheimer disease (AD) rats induced by amyloid β-peptide25-35 (Aβ_25-35) and to investigate the mechanism of NT3 and trkC involved in the pathogenesis of AD. Methods：Thirty male Wistar rats were randomly divided into control and model groups. The AD models were established by the injection of amyloid β-peptide25-35 (Aβ_25-35) into the bilateral hippocampus of rats, while the control rats were subjected to injection of normal saline at the same site. All were tested with the Morris water maze for memory and learning function two weeks after injection. After that, they were killed at the same time. The hippocampal microstructures were observed by an optic microscope. The expressions of NT3 and trkC were detected by an immunohistochemical method. Results： Different expression levels were presented between NT3 and trkC in the different subfields of the hippocampus. The number of NT3 imunoreactive neurons within the hippocampal subfields CA1, CA2 and CA3 in the model group was obviously reduced compared with the control group (P＜ 0.01), while no difference was found in the CA4 and hilar subfields between the two groups (P＞0.05). No difference in the number of trkC imunoreactive neurons in each hippocampal subfield was produced between the two groups (P＞0.05). Conclusion: The decrease of the expression of NT3 but not the down-regulation of its receptor′s in the hippocampus is related to learning and memory dysfunction of AD rats, suggesting an exogenous NT3-supply may counteract the neurotoxicity of β amyloid protein.

Key words: Alzheimer disease, Nerve growth factors, Receptor, trkC, Aβ_25-35