NDLI: Organic Anion Transporter 1 Deficiency Accelerates Learning and Memory Impairment in tg2576 Mice by Damaging Dendritic Spine Morphology and Activity

Content Provider	Springer Nature Link
Author	Wu, Xinlin Zhang, Jianqing Liu, Heng Mian, Yansheng Liang, Birong Xie, Hongbo Zhang, Shijun Sun, Baoguo Zhou, Houming
Copyright Year	2015
Abstract	To investigate whether and how organic anion transporter 1 (OAT1) is involved in the process of Alzheimer’s disease (AD), we crossbred OAT1 knockout mice with tg2576, the widely used AD model mice. Results here showed the heterozygous OAT1-deficient tg2576 mice developed a learning- and memory-related behavior deficiency and higher soluble Abeta amount in early stage (3 months old). Furthermore, the heterozygous mice brain slice also showed impaired long-term potentiation (LTP) and spontaneous excitatory postsynaptic currents (sEPSC). By crossbreeding heterozygous OAT1-deficient tg2576 mice with Thy-1 YFP mice, we got autofluoresced (layer 4/5 cortical neuron) heterozygous mice. By using two-photon microscope in the direct observation of mice brain in vivo or single photon confocal on slices, compared with control tg2576 mice, we found that the OAT1-deficient mice showed a higher spine numbers but with a much lesser maturity extent. Finally, by using glutamate uncaging method, we induced chemical LTP in brain slices and found that OAT1-deficient mice showed abnormal chemical-induced LTP, which meant that the deficient behavior may be caused by abnormal spine morphology and activity. Our results indicated OAT1 may be involved in AD process by regulating spine morphology and activity.
Starting Page	730
Ending Page	738
Page Count	9
File Format	PDF
ISSN	08958696
Journal	Journal of Molecular Neuroscience
Volume Number	56
Issue Number	3
e-ISSN	15591166
Language	English
Publisher	Springer US
Publisher Date	2015-03-01
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	OAT1 Alzheimer’s disease Dendritic spine Learning and memory Neurosciences Neurochemistry Cell Biology Proteomics Neurology
Content Type	Text
Resource Type	Article
Subject	Medicine Cellular and Molecular Neuroscience

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