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成年大鼠中,通过刺激初级传入Aδ纤维对C纤维诱发的脊髓场电位进行长期抑制。

Long-term depression of C-fibre-evoked spinal field potentials by stimulation of primary afferent A delta-fibres in the adult rat.

作者信息

Liu X G, Morton C R, Azkue J J, Zimmermann M, Sandkühler J

机构信息

II. Physiologisches Institut, Universität Heidelberg, Germany.

出版信息

Eur J Neurosci. 1998 Oct;10(10):3069-75. doi: 10.1046/j.1460-9568.1998.00310.x.

Abstract

Long-term potentiation (LTP) of spinal C-fibre-evoked field potentials can be induced by brief electrical stimulation of afferent C-fibres, by natural noxious stimulation of skin or by acute nerve injury. Here, we report that in urethane anaesthetized, adult rats prolonged high frequency burst stimulation of the sciatic nerve at Adelta-fibre strength produced long-term depression (LTD) of C-fibre-evoked field potentials, and also depressed the increased amplitudes of C-fibre-evoked field potentials recorded after LTP had been established (depotentiation). Electrical stimulation of Abeta-fibres failed to induce LTD or depotentiation. In spinalized rats, prolonged Adelta-fibre conditioning stimulation induced LTP rather than LTD of C-fibre-evoked field potentials. Thus, tonic descending inhibition may determine the direction of plastic changes in C-fibre-mediated synaptic transmission. Spinal application of the N-methyl-D-aspartic acid receptor antagonist D-APV blocked induction of LTD in intact rats and LTP in spinalized rats. The presently described LTD and the depotentiation of established LTP of C-fibre-evoked field potentials in spinal dorsal horn may underlie some forms of prolonged analgesia induced by peripheral nerve stimulation procedures.

摘要

脊髓C纤维诱发场电位的长时程增强(LTP)可通过对传入C纤维的短暂电刺激、对皮肤的自然伤害性刺激或急性神经损伤来诱导。在此,我们报告,在乌拉坦麻醉的成年大鼠中,以Aδ纤维强度对坐骨神经进行长时间高频爆发刺激会产生C纤维诱发场电位的长时程抑制(LTD),并且还会抑制在LTP建立后记录到的C纤维诱发场电位的增大幅度(去增强)。对Aβ纤维的电刺激未能诱导LTD或去增强。在脊髓横断的大鼠中,长时间的Aδ纤维条件刺激诱发了C纤维诱发场电位的LTP而非LTD。因此,紧张性下行抑制可能决定C纤维介导的突触传递中可塑性变化的方向。在完整大鼠中脊髓应用N-甲基-D-天冬氨酸受体拮抗剂D-APV可阻断LTD的诱导,而在脊髓横断大鼠中可阻断LTP的诱导。目前所描述的脊髓背角中C纤维诱发场电位的LTD以及已建立的LTP的去增强可能是某些形式的外周神经刺激程序所诱导的长时间镇痛的基础。

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