Ren L-Y, Lu Z-M, Liu M-G, Yu Y-Q, Li Z, Shang G-W, Chen J
Institute for Biomedical Sciences of Pain and Institute for Functional Brain Disorders, Tangdu Hospital, Fourth Military Medical University, #1 Xinsi Road, Baqiao District, Xi'an 710038, PR China.
Neuroscience. 2008 Apr 22;153(1):268-78. doi: 10.1016/j.neuroscience.2008.01.067. Epub 2008 Feb 15.
A wide variety of human and animal experiments suggest that the anterior cingulate cortex (ACC) is one of the key brain substrates subserving higher order processing of noxious information. However, no sufficient data are now available regarding the mediation by ACC of different levels of pain processing as well as its potential descending modulation of spinal nociception. Using the well-developed rat bee venom (BV) model, the present study evaluated the effect of lesions of bilateral ACC on two levels of spontaneous nociceptive behaviors (spinally-processed persistent paw flinching reflex and supraspinally-processed paw lifting/licking) and heat or mechanical hypersensitivity under the inflammatory pain state. In contrast to the sham lesion group (saline microinjection into the ACC), bilateral complete ACC chemical lesions (kainic acid microinjection into the ACC) significantly decreased the BV-induced paw lifting and licking behavior (less time spent by the animal in paw lifting/licking) but produced no influence upon spinally-processed spontaneous paw flinching reflex (no change in number of paw flinches following subcutaneous BV injection). Moreover, the bilateral ACC lesions relieved the BV-evoked primary thermal or mechanical hypersensitivity compared with the sham control group. However, incomplete lesions of bilateral ACC failed to affect the abovementioned pain-related behaviors. No effects were seen on basal pain sensitivity in either group of rats. Motor coordination, as measured by Rota-Rod treadmill test, was not impaired by bilateral ACC lesions. These results implicate that the ACC area of the brain plays differential roles in the mediation of different levels of spontaneous pain-related behaviors. The present study also provides additional evidence for the ACC-mediated descending facilitation of primary hyperalgesia (pain hypersensitivity) identified in the injured area under inflammatory pain state.
各种各样的人类和动物实验表明，前扣带回皮质（ACC）是服务于有害信息高阶处理的关键脑基质之一。然而，目前尚无足够数据说明ACC在不同水平疼痛处理中的介导作用及其对脊髓伤害感受的潜在下行调制。本研究利用成熟的大鼠蜂毒（BV）模型，评估双侧ACC损伤对炎症性疼痛状态下两种自发伤害性行为水平（脊髓处理的持续性爪退缩反射和脊髓上处理的爪抬起/舔舐）以及热或机械超敏反应的影响。与假损伤组（向ACC内微量注射生理盐水）相比，双侧完全性ACC化学损伤（向ACC内微量注射 kainic 酸）显著减少了BV诱导的爪抬起和舔舐行为（动物爪抬起/舔舐所花费的时间减少），但对脊髓处理的自发爪退缩反射没有影响（皮下注射BV后爪退缩次数无变化）。此外，与假对照组相比，双侧ACC损伤减轻了BV诱发的原发性热或机械超敏反应。然而，双侧ACC不完全损伤未能影响上述疼痛相关行为。两组大鼠的基础疼痛敏感性均未受影响。通过转棒式跑步机试验测量的运动协调性，未因双侧ACC损伤而受损。这些结果表明，大脑的ACC区域在介导不同水平的自发疼痛相关行为中发挥着不同作用。本研究还为ACC介导的在炎症性疼痛状态下损伤区域中识别出的原发性痛觉过敏（疼痛超敏反应）的下行易化作用提供了额外证据。
