Role of the Rostral Medial Medulla in the Development of Primary and Secondary Hyperalgesia after Incision in the Rat

Role of the Rostral Medial Medulla in the Development of Primary and Secondary Hyperalgesia after Incision in the Rat
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DOI:
10.1097/00000542-200205000-00019
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发表时间:
2002-05
期刊:
影响因子:
8.8
通讯作者:
Z. Bosnjak;E. Pogatzki;M. Urban;T. Brennan;G. Gebhart
Z. Bosnjak;E. Pogatzki;M. Urban;T. Brennan;G. Gebhart
中科院分区:
医学1区
文献类型:
--
作者:
Z. Bosnjak;E. Pogatzki;M. Urban;T. Brennan;G. Gebhart

文献摘要

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在持续性炎症性、神经性和内脏痛模型中,来自延髓头端内侧区(RMM)的下行影响导致继发性痛觉过敏。当前的研究检查了RMM的下行抑制或促进是否会调节大鼠后肢切口后的原发性和继发性痛觉过敏。方法采用体细胞选择性神经毒素鹅膏蕈氨酸造成大鼠双侧RMM损伤,分别于足底或腓肠肌切口后5 d观察RMM损伤对原发性和继发性痛觉过敏的影响。结果足底切口降低了对邻近切口的von Frey细丝的退缩阈值(原发性点状痛觉过敏)。在RMM损伤和假手术大鼠中的退缩阈值相同。在两组中,足底切口后对钝性机械刺激的反应频率增加(原发性非点状痛觉过敏)。非点状痛觉过敏是更大的损伤大鼠术后第2天,所有其他措施没有不同。足底切口后的原发性热痛觉过敏不受RMM损伤的调制。腓肠肌切开后继发性点状痛敏不受RMM损伤的影响。腓肠肌切口没有产生继发性非点状或热痛觉过敏的RMM损伤或假手术大鼠。结论切口后的原发性和继发性痛觉过敏不受RMM的下行影响。腓肠肌切开后,RMM对继发性痛觉过敏的下行易化影响的贡献不足,这支持了以下观点:与炎症性和神经性疼痛相比,切口诱导的疼痛涉及不同的机制。
Background Descending influences from the rostral medial medulla (RMM) contribute to secondary hyperalgesia in persistent inflammatory, neuropathic, and visceral pain models. The current study examined if descending inhibition or facilitation from the RMM modulates primary and secondary hyperalgesia after incision in the rat hind limb. Methods Bilateral RMM lesions were produced using the soma-selective neurotoxin ibotenic acid, and the effect of RMM lesion was examined on primary and secondary hyperalgesia 5 days after a plantar or gastrocnemius incision, respectively. Results Plantar incision reduced withdrawal thresholds to von Frey filaments applied adjacent to the incision (primary punctate hyperalgesia). The withdrawal thresholds were the same in RMM-lesioned and sham-operated rats. The response frequency to a blunt mechanical stimulus after plantar incision was increased (primary nonpunctate hyperalgesia) in both groups. Nonpunctate hyperalgesia was greater in lesioned rats on postoperative day 2 only; all other measures were not different. Primary heat hyperalgesia after plantar incision was not modulated by RMM lesion. Secondary punctate hyperalgesia after gastrocnemius incision was not affected by RMM lesion. Gastrocnemius incision did not produce secondary nonpunctate or heat hyperalgesia in either RMM lesion or sham rats. Conclusion Primary and secondary hyperalgesia after an incision were not modulated by descending influence from the RMM. The lack of contribution of descending facilitatory influences from the RMM to secondary hyperalgesia after gastrocnemius incision supports the notion that incision-induced pain involves dissimilar mechanisms compared with inflammatory and neuropathic pain.