期刊
NEUROSCIENCE LETTERS
卷 502, 期 1, 页码 30-32出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2011.07.018
关键词
Gap junctions; Connexin 36; LTP; Hippocampus; NMDA receptors
资金
- NIH [R01 NS064256]
- University of Kansas Medical Center
In the mammalian CNS, deletion of neuronal gap junction protein, connexin 36 (Cx36), causes deficiencies in learning and memory. Here we tested whether Cx36 deletion affects the hippocampal long-term potentiation (LTP), which is considered as a cellular model of learning and memory mechanisms. We report that in acute slices of the hippocampal CA1 area, LTP is reduced in Cx36 knockout mice as compared to wild-type mice. Western blot analysis of NMDA receptor subunits indicates a higher NR2A/NR2B ratio in Cx36 knockout mice, indicating that there is shift in the threshold for LTP induction in knockout animals. Data suggest a possibility that learning and memory deficiencies in Cx36 knockout mice are due to deficiencies in LTP mechanisms. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
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