Froc D J, Racine R J
Department of Psychology, McMaster University, Hamilton, Ontario L8S 4K1, Canada.
Neuroscience. 2004;129(2):273-81. doi: 10.1016/j.neuroscience.2004.06.069.
Bidirectional modifications in synaptic efficacy are central components in recent models of cortical learning and memory, and we previously demonstrated both long-term synaptic potentiation (LTP) and long-term synaptic depression (LTD) in the neocortex of the unanaesthetized adult rat. Here, we have examined the effects of N-methyl-D-aspartate receptor (NMDAR) blockade on the induction of LTD, LTP, and depotentiation of field potentials evoked in sensorimotor cortex by stimulation of the white matter in the adult, freely moving rat. High frequency (300 Hz) stimulation (HFS) was used to induce LTP and prolonged, low-frequency (1 Hz) stimulation was used to induce either depotentiation or LTD. LTD was expressed as a reduction in the amplitude of the short and long-latency field potential components, while depotentiation was expressed as a decrease in the amplitude of a previously enhanced late component. Under NMDAR blockade, HFS failed to induce LTP and instead produced a depression effect similar to LTD. Following washout of the drug, HFS induced a normal LTP effect. Unlike LTP, LTD and depotentiation were found to be NMDAR-independent in the neocortex of the freely moving rat.
突触效能的双向修饰是近期皮质学习和记忆模型的核心组成部分,我们之前在未麻醉的成年大鼠新皮质中证明了长时程突触增强(LTP)和长时程突触抑制(LTD)。在此,我们研究了N-甲基-D-天冬氨酸受体(NMDAR)阻断对成年自由活动大鼠感觉运动皮质中白质刺激诱发的场电位LTD、LTP和去增强的诱导作用。高频(300Hz)刺激(HFS)用于诱导LTP,而长时间低频(1Hz)刺激用于诱导去增强或LTD。LTD表现为短潜伏期和长潜伏期场电位成分的幅度降低,而去增强表现为先前增强的晚期成分的幅度降低。在NMDAR阻断下,HFS未能诱导LTP,反而产生了类似于LTD的抑制作用。药物洗脱后,HFS诱导出正常的LTP效应。与LTP不同,在自由活动大鼠的新皮质中,LTD和去增强被发现是不依赖NMDAR的。