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Aggravated chronic brain injury after focal cerebral ischemia in aquaporin-4-deficient mice
Authors:Shi Wen-Zhen  Qi Ling-Ling  Fang San-Hua  Lu Yun-Bi  Zhang Wei-Ping  Wei Er-Qing
Affiliation:a School of Biological Sciences, College of Natural Sciences, Seoul National University, Seoul 151-742, Republic of Korea
b Department of Biology, Department of Life and Nanopharmaceutical Sciences, Kyunghee University, Seoul 130-701, Republic of Korea
c School of Biological Sciences, Nanyang Technological University, 60 Nanyang Drive, Singapore 637551
d Department of Chemistry and Nano Science, Department of Brain & Cognitive Sciences, Ewha Woman's University, Seoul 120-750, Republic of Korea
Abstract:
Late-phase long-term potentiation (L-LTP) of excitatory synaptic transmission at thalamic input synapses onto the lateral amygdala (T-LA synapses) has been proposed as a cellular substrate for long-term fear memory. This notion is evidenced primarily by previous reports in which the same pharmacological treatments block both T-LA L-LTP and the consolidation of fear memory. In this study, we report that fear conditioning occludes L-LTP at T-LA synapses in brain slices prepared after fear memory consolidation. L-LTP was restored either when synaptic depotentiation was induced prior to L-LTP induction in brain slices prepared from conditioned rats or when brain slices were prepared from conditioned rats that had been exposed to subsequent fear extinction, which is a behavior paradigm known to induce in vivo synaptic depotentiation at T-LA synapses. These results suggest that fear conditioning recruits L-LTP-like mechanisms that are reversible and saturable at T-LA synapses.
Keywords:Amygdala   Synaptic plasticity   Learning and memory   Late-phase LTP   Depotentiation   Fear conditioning   Fear extinction
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