Open AccessBlocking beta 2-adrenergic receptor inhibits dendrite ramification in a mouse model of Alzheimer's disease
Author(s) -
Qin Wu,
Jie Sun,
Xiang-He Song,
Jing Wang,
Cunquan Xiong,
Feixiang Teng,
Cuixiang Gao
Publication year - 2017
Publication title -
neural regeneration research/neural regeneration research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.93
H-Index - 38
eISSN - 1876-7958
pISSN - 1673-5374
DOI - 10.4103/1673-5374.215261
Subject(s) - synaptophysin , hippocampal formation , dendrite (mathematics) , medicine , receptor , endocrinology , morris water navigation task , adrenergic receptor , amyloid precursor protein , amyloid beta , genetically modified mouse , chemistry , western blot , alzheimer's disease , neuroscience , biology , transgene , immunohistochemistry , biochemistry , disease , geometry , mathematics , gene
Dendrite ramification affects synaptic strength and plays a crucial role in memory. Previous studies revealed a correlation between beta 2-adrenergic receptor dysfunction and Alzheimer's disease (AD), although the mechanism involved is still poorly understood. The current study investigated the potential effect of the selective β 2 -adrenergic receptor antagonist, ICI 118551 (ICI), on Aβ deposits and AD-related cognitive impairment. Morris water maze test results demonstrated that the performance of AD-transgenic (TG) mice treated with ICI (AD-TG/ICI) was significantly poorer compared with NaCl-treated AD-TG mice (AD-TG/NaCl), suggesting that β 2 -adrenergic receptor blockage by ICI might reduce the learning and memory abilities of mice. Golgi staining and immunohistochemical staining revealed that blockage of the β 2 -adrenergic receptor by ICI treatment decreased the number of dendritic branches, and ICI treatment in AD-TG mice decreased the expression of hippocampal synaptophysin and synapsin 1. Western blot assay results showed that the blockage of β 2 -adrenergic receptor increased amyloid-β accumulation by downregulating hippocampal α-secretase activity and increasing the phosphorylation of amyloid precursor protein. These findings suggest that blocking the β 2 -adrenergic receptor inhibits dendrite ramification of hippocampal neurons in a mouse model of AD.