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

NMDA receptor involvement in neuroplastic changes induced by neonatal capsaicin treatment in trigeminal nociceptive neurons.
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NMDA 受体参与新生儿辣椒素治疗三叉神经伤害性神经元引起的神经塑性变化。

DOI:
10.1152/jn.1997.78.5.2799
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发表时间:
1997
期刊:
Journal of neurophysiology.
影响因子:
--
通讯作者:
Sessle,BJ
Sessle,BJ
中科院分区:
--
文献类型:
--
作者:
Chiang,CY;Hu,JW;Sessle,BJ

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Jiang, Chen Yu, James W. Hu, and Barry J. Sessle.NMDA 受体参与新生儿辣椒素治疗三叉神经伤害性神经元引起的神经塑性变化。 Neurophysiol.78: 2799–2803, 1997。本研究探讨了 1) 新生儿 C 纤维传入神经的丧失是否会导致成年大鼠三叉神经尾亚核(髓背角)中伤害感受神经元的机械感受场 (RF) 特性和自发活动的神经塑性变化,以及 2) N-甲基-d-天冬氨酸 (NMDA) 受体机制参与这些神经塑性变化。与媒介物治疗(即对照,CON)大鼠相比,辣椒素治疗(CAP)大鼠的神经元自发活动和 RF 大小本身显着增加,但这些神经塑性变化可以通过非竞争性 NMDA 受体拮抗剂 MK-801(1 mg/kg,静脉注射)显着减少; MK-801 给药后 CON 大鼠和媒介物(盐水,静脉注射)后 CAP 大鼠中 RF 大小和自发活动保持不变。鞘内注射 7-氯犬脲酸 (5 μg/10 μl)(NMDA 受体上对马钱子碱不敏感的甘氨酸结合位点的拮抗剂)也能显着降低 CAP 大鼠的神经元 RF 大小和自发活动,但对 CON 大鼠没有影响。这些数据证明 C 纤维传入在塑造伤害性神经元的特性中发挥作用,并且神经塑性变化涉及 NMDA 受体机制。
Chiang, Chen Yu, James W. Hu, and Barry J. Sessle.NMDA receptor involvement in neuroplastic changes induced by neonatal capsaicin treatment in trigeminal nociceptive neurons.J. Neurophysiol.78: 2799–2803, 1997. This study examines whether1) 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 that2)N-methyl-d-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 μg/10 μl), an antagonist of strychnine-insensitive glycine binding 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.