genetic enhancement of memory and long-term potentiation but not ca1 long-term depression in nr2b transgenic rats基因增强记忆和长期势差但不是ca1 nr2b转基因大鼠的长期萧条.pdfVIP
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genetic enhancement of memory and long-term potentiation but not ca1 long-term depression in nr2b transgenic rats基因增强记忆和长期势差但不是ca1 nr2b转基因大鼠的长期萧条
Genetic Enhancement of Memory and Long-Term
Potentiation but Not CA1 Long-Term Depression in NR2B
Transgenic Rats
1,2. 2. 1 1,3 2,3 2
Deheng Wang , Zhenzhong Cui , Qingwen Zeng , Hui Kuang , L. Phillip Wang , Joe Z. Tsien *,
Xiaohua Cao1*
1 Shanghai Institute of Brain Functional Genomics, the Key Laboratories of MOE and STCSM and College of Life Sciences, East China Normal University, Shanghai, China,
2 Brain and Behavior Discovery Institute and Department of Neurology, School of Medicine, Medical College of Georgia, Augusta, Georgia, United States of America,
3 Yunnan Banna Primate Model Research Center, Xishuang-Banna, Yunnan, China
Abstract
One major theory in learning and memory posits that the NR2B gene is a universal genetic factor that acts as rate-limiting
molecule in controlling the optimal NMDA receptor’s coincidence-detection property and subsequent learning and memory
function across multiple animal species. If so, can memory function be enhanced via transgenic overexpression of NR2B in
another species other than the previously reported mouse species? To examine these crucial issues, we generated
transgenic rats in which NR2B is overexpressed in the cortex and hippocampus and investigated the role of NR2B gene in
NMDA receptor-mediated synaptic plasticity and memory functions by combining electrophysiological technique with
behavioral measurements. We found that overexpression of the NR2B subunit had no effect on CA1-LTD, but rather resulted
in enhanced CA1-LTP and improved memory performances in novel object recognition test, spatial water maze, and
delayed-to-nonmatch working memory test. Our slices recordings
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