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Mol. Cells 2011; 32(2): 197-201

Published online June 1, 2011

https://doi.org/10.1007/s10059-011-0077-8

© The Korean Society for Molecular and Cellular Biology

Pathway-Specific Alteration of Synaptic Plastic-ity in Tg2576 Mice

Jung Hoon Jung, Kyongman An, Oh Bin Kwon, Hye-sun Kim1, and Joung-Hun Kim*

Department of Life Science, Pohang University of Science and Technology (POSTECH), Pohang 790-784, Korea, 1Department of Pharmacology, Seoul National University, College of Medicine, Seoul 110-799, Korea

Correspondence to : *Correspondence: joungkim@postech.ac.kr

Received: April 19, 2011; Revised: May 25, 2011; Accepted: May 25, 2011

Abstract

Various animal models of Alzheimer disease (AD) are cha- racterized by deficits in spatial memory that are causally related to altered synaptic function and impairment of long-term potentiation (LTP) in the hippocampus. In Tg2576 AD mice, we compared LTP in 2 major hippocampal path- ways, Schaffer collateral (SC) and mossy fiber (MF) pathways. Whereas LTP was completely abolished in the SC pathway of Tg2576 mice, we found no decrease in LTP induced by stimulation of the MF pathway. In fact, we found that in the MF pathway, LTP was slightly, but sig-nificantly, enhanced compared with that in the MF pathway of WT littermates. This pathway-specific impair-ment of LTP is not attributable to alterations in transmitter release, as indicated by an unaltered paired-pulse ratio. These results suggest that the spatial memory deficits normally seen in AD models arise primarily from LTP im-pairment at the SC pathway.

Keywords Alzheimer’s disease, long-term potentiation, mossy fiber pathway, schaffer collateral pathway, Tg2576

Article

Research Article

Mol. Cells 2011; 32(2): 197-201

Published online August 31, 2011 https://doi.org/10.1007/s10059-011-0077-8

Copyright © The Korean Society for Molecular and Cellular Biology.

Pathway-Specific Alteration of Synaptic Plastic-ity in Tg2576 Mice

Jung Hoon Jung, Kyongman An, Oh Bin Kwon, Hye-sun Kim1, and Joung-Hun Kim*

Department of Life Science, Pohang University of Science and Technology (POSTECH), Pohang 790-784, Korea, 1Department of Pharmacology, Seoul National University, College of Medicine, Seoul 110-799, Korea

Correspondence to:*Correspondence: joungkim@postech.ac.kr

Received: April 19, 2011; Revised: May 25, 2011; Accepted: May 25, 2011

Abstract

Various animal models of Alzheimer disease (AD) are cha- racterized by deficits in spatial memory that are causally related to altered synaptic function and impairment of long-term potentiation (LTP) in the hippocampus. In Tg2576 AD mice, we compared LTP in 2 major hippocampal path- ways, Schaffer collateral (SC) and mossy fiber (MF) pathways. Whereas LTP was completely abolished in the SC pathway of Tg2576 mice, we found no decrease in LTP induced by stimulation of the MF pathway. In fact, we found that in the MF pathway, LTP was slightly, but sig-nificantly, enhanced compared with that in the MF pathway of WT littermates. This pathway-specific impair-ment of LTP is not attributable to alterations in transmitter release, as indicated by an unaltered paired-pulse ratio. These results suggest that the spatial memory deficits normally seen in AD models arise primarily from LTP im-pairment at the SC pathway.

Keywords: Alzheimer’s disease, long-term potentiation, mossy fiber pathway, schaffer collateral pathway, Tg2576

Mol. Cells
Jan 31, 2023 Vol.46 No.1, pp. 1~67
COVER PICTURE
RNAs form diverse shapes and play multiple functions as central molecules of gene expression. In this special issue on RNA, seven minireviews illustrate how basic concepts and recent RNA biology findings are transformed into new and exciting RNA therapeutics.

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