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脊髓N-甲基-D-天冬氨酸受体阻断可防止大鼠脊髓背角C纤维诱发电位的长期增强。

Long-term potentiation of C-fiber-evoked potentials in the rat spinal dorsal horn is prevented by spinal N-methyl-D-aspartic acid receptor blockage.

作者信息

Liu X G, Sandkühler J

机构信息

II. Physiologisches Institut, Universität Heidelberg, Germany.

出版信息

Neurosci Lett. 1995 May 19;191(1-2):43-6. doi: 10.1016/0304-3940(95)11553-0.

Abstract

Long-term potentiation (LTP) of synaptic potentials is a fundamental mechanism of memory formation in the hippocampus. Here, we have characterized long-term changes of field potentials which were evoked in the lumbar spinal dorsal horn by supramaximal electrical stimulation of the sciatic nerve in urethane anesthetized rats. The field potentials had high thresholds (> or = 7 V), long latencies (90-130 ms, corresponding to conduction velocities between 1.2 and 0.85 m/s) and were not affected by spinalization (at C5-C6) or muscle relaxation (with pancuronium), i.e. the potentials were probably evoked by afferent C-fibers. Tetanic electrical stimulation (0.5 ms pulses, 30-40 V, 100 Hz, given in 4 trains of 1 s duration at 10 s intervals) of sciatic nerve induced in all 9 rats tested a LTP of amplitude of the C-fiber-evoked potential throughout recording periods which lasted between 4 and 9 h. Mean potentiation ranged from +71% to +174%. Superfusion of spinal cord with N-methyl-D-aspartic acid (NMDA) receptor antagonist D-(-)-4-(3-phosphonopropyl)piperazine-2-carboxylic (500 nM), which has little effect on the amplitude of C-fiber-evoked potentials, completely blocked LTP induced by tetanic stimulation in all five rats tested. Superfusion of spinal cord with NMDA (1 microM, 10 microM or 50 microM) induced LTP in only 2 out of 8 rats. This is the first report showing that LTP of C-fiber-evoked field potentials in the spinal dorsal horn in vivo may last for more than 8 h. This LTP in the spinal dorsal horn may underlie plastic changes of spinal nociception.

摘要

突触电位的长时程增强(LTP)是海马体中记忆形成的基本机制。在此,我们描述了在氨基甲酸乙酯麻醉的大鼠中,通过坐骨神经的超强电刺激在腰脊髓背角诱发的场电位的长期变化。场电位具有高阈值(≥7 V)、长潜伏期(90 - 130毫秒,对应传导速度在1.2至0.85米/秒之间),并且不受脊髓横断(在C5 - C6水平)或肌肉松弛(使用泮库溴铵)的影响,即这些电位可能是由传入的C纤维诱发的。对坐骨神经进行强直电刺激(0.5毫秒脉冲,30 - 40 V,100 Hz,以10秒间隔给予4组持续1秒的刺激),在所有9只受试大鼠中,在整个持续4至9小时的记录期间,均诱发了C纤维诱发电位幅度的LTP。平均增强幅度在 +71%至 +174%之间。用对C纤维诱发电位幅度影响较小的N - 甲基 - D - 天冬氨酸(NMDA)受体拮抗剂D - (-)-4-(3 - 膦酰基丙基)哌嗪 - 2 - 羧酸(500 nM)灌注脊髓,在所有5只受试大鼠中完全阻断了强直刺激诱导的LTP。用NMDA(1 microM、10 microM或50 microM)灌注脊髓,仅在8只大鼠中的2只中诱发了LTP。这是首次报道显示,体内脊髓背角C纤维诱发场电位的LTP可能持续超过8小时。脊髓背角的这种LTP可能是脊髓痛觉可塑性变化的基础。

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