DMXB (GTS-21) ameliorates the cognitive deficits in beta amyloid(25-35(-) ) injected mice through preventing the dysfunction of alpha7 nicotinic receptor

Journal of Neuroscience Research
Lei ChenLing Chen

Abstract

Intracerebroventricular injection of beta-amyloid(25-35) (Abeta(25-35)) in mice leads to cognitive deficits with the dysfunction of alpha7 nicotinic acetylcholine receptor (alpha7nAChR) within 1-2 weeks in a dose-dependent manner. The present study focused on the effect of DMXB, a selective alpha7nAChR agonist, on Abeta(25-35) (3 nmol)-impaired spatial memory and alpha7nAChR function. We found that the treatment with DMXB on days 1-10 after Abeta(25-35) injection dose-dependently prevented Abeta(25-35)-induced impairment of acquisition performance and probe trail test in Morris water maze. Importantly, the treatment with DMXB (1 mg/kg) perfectly prevented Abeta(25-35)-induced depression of alpha7nAChR response, which was associated with improving the probability of presynaptic glutamate release and the induction of high-frequency stimulation (HFS)-dependent long-term potentiation (LTP) in hippocampal Schaffer collaterale-CA1 synapse. Furthermore, although either the basal level of extracellular signal-regulated kinase 2 (ERK2) or its phosphorylation in the hippocampus had no difference between control and Abeta(25-35) mice, the Abeta(25-35) injection significantly attenuated HFS-triggered increase in ERK2 phosphorylation. The t...Continue Reading

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Citations

Jan 22, 2011·International Journal of Alzheimer's Disease·Jin WuKenji Hashimoto
Apr 3, 2015·Molecular Neurobiology·Zi-Xuan WangJin-Tai Yu
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Oct 1, 2015·Pharmacological Reviews·Daniel BertrandDiana Donnelly-Roberts
May 20, 2021·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Chenghuan SongHao Wang

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