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前扣带回皮质通过背侧网状核参与对疼痛的下行易化调制。

Anterior cingulate cortex contributes to the descending facilitatory modulation of pain via dorsal reticular nucleus.

作者信息

Zhang Ling, Zhang Yuqiu, Zhao Zhi-Qi

机构信息

Institute of Neurobiology, Fudan University, Shanghai 200433, P R China.

出版信息

Eur J Neurosci. 2005 Sep;22(5):1141-8. doi: 10.1111/j.1460-9568.2005.04302.x.

Abstract

Supraspinal centres biphasically modulate spinal nociceptive transmission, including descending inhibition and facilitation. Recent studies have revealed that descending facilitatory modulation is a key mechanism underlying induction and maintenance of neuropathic and inflammatory pain. The anterior cingulate cortex (ACC) is not only involved in the transmission of pain sensation but also plays a role in processing pain-related emotion. The ACC also widely connects with relevant regions of the descending modulation system. Here we used electrophysiological and behavioural techniques to study the possible pathways behind the modulation of spinal nociceptive transmission from the ACC. C-fibre-evoked field potentials in the spinal dorsal horn were produced by electrical stimulation of the sciatic nerve at an intensity high enough to excite C fibres, and paw withdrawal latencies (PWLs) to noxious heating were recorded. The results showed that high-frequency tetanic electrical stimulation of the ACC both unilaterally enhanced the C-fibre-evoked field potentials in the spinal dorsal horn and bilaterally shortened PWLs, indicating a facilitation of spinal nociception. A similar effect was observed after microinjection of N-methyl-d-aspartic acid (NMDA; 10 nm, 1 microL) or homocysteic acid (HCA; 0.1 m, 1 microL) into the ACC. When the dorsal reticular nucleus (DRt) was electrolytically lesioned, ACC-induced facilitation of spinal nociception was blocked. These results imply that: (i) activation of the ACC may facilitate spinal nociception; (ii) NMDA receptors in the ACC may be involved in descending facilitation; and (iii) the DRt plays a crucial role in mediating ACC-induced facilitation of spinal nociception.

摘要

脊髓上中枢对脊髓伤害性感受传递具有双相调节作用,包括下行抑制和易化。最近的研究表明,下行易化调节是神经性疼痛和炎性疼痛诱导及维持的关键机制。前扣带回皮质(ACC)不仅参与痛觉传递,还在疼痛相关情绪的处理中发挥作用。ACC还与下行调节系统的相关区域广泛连接。在此,我们使用电生理和行为学技术研究ACC调节脊髓伤害性感受传递背后的可能途径。通过以足以兴奋C纤维的强度电刺激坐骨神经,在脊髓背角产生C纤维诱发的场电位,并记录对有害热刺激的爪缩潜伏期(PWL)。结果表明,对ACC进行高频强直电刺激,既能单侧增强脊髓背角C纤维诱发的场电位,又能双侧缩短PWL,表明对脊髓伤害性感受有易化作用。向ACC微量注射N-甲基-D-天冬氨酸(NMDA;10 nM,1 μL)或高半胱氨酸(HCA;0.1 M,1 μL)后也观察到类似效果。当对背侧网状核(DRt)进行电解损伤时,ACC诱导的脊髓伤害性感受易化被阻断。这些结果表明:(i)ACC的激活可能促进脊髓伤害性感受;(ii)ACC中的NMDA受体可能参与下行易化;(iii)DRt在介导ACC诱导的脊髓伤害性感受易化中起关键作用。

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