Department of Physiology, Neural Systems and Plasticity Research Group, University of Saskatchewan, 9 Campus Drive, Saskatoon, SK, S7N 5A5, Canada.
Hippocampus. 2010 Dec;20(12):1327-31. doi: 10.1002/hipo.20738.
Cognitive functions such as learning and memory are widely believed to depend on patterns of short- and long-term synaptic plasticity. Factors, such as acute stress, which affect learning and memory, may do so by altering patterns of synaptic plasticity in distinct neural circuits. Numerous studies have examined the effects of acute stress on long-term synaptic plasticity; however, few have examined its influence on short-term plasticity. The present experiments directly assessed the effects of acute stress on short-term synaptic plasticity as measured by paired pulse facilitation (PPF) of excitatory postsynaptic potentials recorded from rat dorsal hippocampus (dHip) in vivo. Long-term potentiation (LTP) was also examined. Acute stress induced by exposure to an elevated platform impaired PPF and LTP in the dHip. Pretreatment of rats exposed to stress with mifepristone (RU38486; 10 mg kg⁻¹) blocked the stress-induced impairment of both PPF and LTP. These data demonstrate that activation of glucocorticoid receptors during acute stress disrupts normal patterns of both PPF and LTP in the dHip.
认知功能，如学习和记忆，被广泛认为依赖于短期和长期突触可塑性的模式。影响学习和记忆的因素，如急性应激，可能通过改变不同神经回路中的突触可塑性模式来实现。许多研究已经研究了急性应激对长期突触可塑性的影响；然而，很少有研究关注其对短期可塑性的影响。本实验直接评估了急性应激对大鼠背侧海马（dHip）体内记录的兴奋性突触后电位的成对脉冲易化（PPF）的短期突触可塑性的影响。还研究了长时程增强（LTP）。暴露在高架平台上的急性应激诱导损伤了 dHip 中的 PPF 和 LTP。用米非司酮（RU38486；10mg/kg）预处理应激大鼠可阻断应激引起的 PPF 和 LTP 损伤。这些数据表明，急性应激期间糖皮质激素受体的激活破坏了 dHip 中 PPF 和 LTP 的正常模式。
