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NMDA受体参与新生期辣椒素处理诱导的三叉神经伤害性神经元的神经可塑性变化。

NMDA receptor involvement in neuroplastic changes induced by neonatal capsaicin treatment in trigeminal nociceptive neurons.

作者信息

Chiang C Y, Hu J W, Sessle B J

机构信息

Faculty of Dentistry, University of Toronto, Toronto, Ontario M5G 1G6, Canada.

出版信息

J Neurophysiol. 1997 Nov;78(5):2799-803. doi: 10.1152/jn.1997.78.5.2799.

DOI:10.1152/jn.1997.78.5.2799
PMID:9356428
Abstract

NMDA receptor involvement in neuroplastic changes induced by neonatal capsaicin treatment in trigeminal nociceptive neurons. J. Neurophysiol. 78: 2799-2803, 1997. This study examines whether 1) the neonatal loss of C-fiber afferents results in neuroplastic changes in the mechanoreceptive field (RF) properties and spontaneous activity of nociceptive neurons in trigeminal subnucleus caudalis (medullary dorsal horn) of adult rats, and that 2) N-methyl--aspartic acid (NMDA) receptor mechanisms are involved in these neuroplastic changes. Compared with vehicle-treated (i.e., control, CON) rats, capsaicin-treated (CAP) rats showed a marked increase in neuronal spontaneous activity and RF size per se, but these neuroplastic changes could be significantly reduced by MK-801 (1 mg/kg, iv), a noncompetitive NMDA receptor antagonist; RF size and spontaneous activity remained unchanged in CON rats after MK-801 administration and in CAP rats after vehicle (saline, iv). Administration of 7-chlorokynurenic acid intrathecally (5 microgram/10 microliter), an antagonist of strychnine-insensitive glycine bindin sites on the NMDA receptor, also significantly reduced neuronal RF size and spontaneous activity in CAP rats, but not in CON rats. These data provide evidence that C-fiber afferents play a role in shaping the properties of nociceptive neurons and that the neuroplastic changes involve NMDA receptor mechanisms.

摘要

N-甲基-D-天冬氨酸(NMDA)受体参与新生大鼠三叉神经伤害性神经元中辣椒素诱导的神经可塑性变化。《神经生理学杂志》78: 2799 - 2803, 1997年。本研究旨在探讨:1)成年大鼠三叉神经尾侧亚核(延髓背角)中伤害性神经元的机械感受野(RF)特性和自发活动是否因新生期C纤维传入纤维的缺失而发生神经可塑性变化;以及2)N-甲基-D-天冬氨酸(NMDA)受体机制是否参与这些神经可塑性变化。与接受载体处理(即对照,CON)的大鼠相比,接受辣椒素处理(CAP)的大鼠神经元自发活动和RF大小本身显著增加,但这些神经可塑性变化可被非竞争性NMDA受体拮抗剂MK-801(1毫克/千克,静脉注射)显著降低;MK-801给药后CON大鼠的RF大小和自发活动保持不变,生理盐水(静脉注射)给药后CAP大鼠的RF大小和自发活动也保持不变。鞘内注射7-氯犬尿氨酸(5微克/10微升),一种NMDA受体上士的宁不敏感甘氨酸结合位点的拮抗剂,也显著降低了CAP大鼠的神经元RF大小和自发活动,但对CON大鼠无此作用。这些数据表明C纤维传入纤维在塑造伤害性神经元特性方面发挥作用,且神经可塑性变化涉及NMDA受体机制。

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