Tan Tao, Zhang Bao-Liang, Tian Xin
Institute of Biomedical Engineering, Tianjin Medical University, Tianjin, China.
Sheng Li Xue Bao. 2011 Jun 25;63(3):225-32.
Synaptic plasticity, including long-term potentiation (LTP) and long-term depression (LTD), is widely considered as one of the major mechanisms underlying learning and memory. This study explored hippocampal synaptic plasticity and spatial memory formation of an Alzheimer's disease (AD) rat model established by intrahippocampal injection of oligomeric Aβ(1-42). Twenty four Sprague-Dawley rats at 2.5 months of age were randomly divided into AD and control groups, and were bilaterally injected with 5 μg oligomeric Aβ(1-42) or normal saline into dentate gyrus (DG) of hippocampus. Morris water maze test was used to observe the capability of learning and memory of two groups, 30 d after injection. To investigate the variations of paired-pulse facilitation (PPF) and range of synaptic plasticity, field potentials were recorded in the DG of the dorsal hippocampus by stimulating the perforant path (PP). The results showed that oligomeric Aβ(1-42) obviously impaired spatial memory formation in rats (P < 0.05). Furthermore, oligomeric Aβ(1-42) reduced the PPF ratio (P < 0.05) and hippocampal LTP formation (P < 0.05), while facilitated the hippocampal LTD formation (P < 0.05). These data suggest that chronic Aβ aggregation impairs synaptic plasticity of hippocampal PP-DG pathway, which may be involved in the spatial memory deficit in AD rats.
突触可塑性，包括长时程增强（LTP）和长时程抑制（LTD），被广泛认为是学习和记忆的主要机制之一。本研究探讨了通过海马内注射寡聚Aβ（1-42）建立的阿尔茨海默病（AD）大鼠模型的海马突触可塑性和空间记忆形成。将24只2.5月龄的Sprague-Dawley大鼠随机分为AD组和对照组，双侧海马齿状回（DG）注射5μg寡聚Aβ（1-42）或生理盐水。注射30天后，采用Morris水迷宫试验观察两组大鼠的学习和记忆能力。为了研究双脉冲易化（PPF）和突触可塑性范围的变化，通过刺激穿通通路（PP）在背侧海马DG记录场电位。结果表明，寡聚Aβ（1-42）明显损害大鼠的空间记忆形成（P<0.05）。此外，寡聚Aβ（1-42）降低了PPF比率（P<0.05）和海马LTP形成（P<0.05），同时促进了海马LTD形成（P<0.05）。这些数据表明，慢性Aβ聚集损害海马PP-DG通路的突触可塑性，这可能与AD大鼠的空间记忆缺陷有关。
