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脊髓中蛋白激酶C的激活通过激活谷氨酸受体产生机械性痛觉过敏,但不介导慢性肌肉诱导的痛觉过敏。

Activation of protein kinase C in the spinal cord produces mechanical hyperalgesia by activating glutamate receptors, but does not mediate chronic muscle-induced hyperalgesia.

作者信息

Sluka K A, Audette K M

机构信息

Graduate Program in Physical Therapy and Rehabilitation Science, Pain Research Program, Neuroscience Graduate Program, University of Iowa, Iowa City, IA 52241, USA.

出版信息

Mol Pain. 2006 Apr 3;2:13. doi: 10.1186/1744-8069-2-13.

Abstract

BACKGROUND

Protein kinase C (PKC) in the spinal cord appears to mediate chronic injury-induced pain, but not acute nociceptive pain. Muscle insult results in increased release of glutamate spinally, and hyperalgesia that is reversed by spinal blockade of NMDA and non-NMDA glutamate receptors. Therefore, we hypothesized that spinal activation of PKC 1) mediates the late phase of hyperalgesia 1 week after muscle insult, and 2) produces mechanical hyperalgesia through activation of NMDA and non-NMDA glutamate receptors.

RESULTS

Rats were implanted with intrathecal catheters for delivery of drugs directly to the spinal cord. Mechanical withdrawal thresholds of the paw were determined using von Frey filaments. Intrathecal phorbol 12,13 dibutyrate (PDBu) produced a dose-dependent decrease in the mechanical withdrawal threshold of the paw that was prevented by pretreatment with the PKC inhibitor, GF109203X. Pretreatment with an NMDA receptor antagonist (AP5) or a AMPA/kainate receptor antagonist (NBQX) prevented the decrease in mechanical withdrawal threshold by PDBu. Two injections of acidic saline in the gastrocnemius muscle decreased the mechanical withdrawal thresholds of the paw bilaterally 24 h and 1 week after the second injection. However, blockade PKC in the spinal cord had no effect on the decreased withdrawal thresholds of the paw when compared to vehicle controls.

CONCLUSION

Spinal activation of PKC produces mechanical hyperalgesia of the paw that depends on activation of NMDA and non-NMDA receptors. Chronic muscle-induced mechanical hyperalgesia, on the other hand, does not utilize spinal PKC.

摘要

背景

脊髓中的蛋白激酶C(PKC)似乎介导慢性损伤诱导的疼痛,但不介导急性伤害性疼痛。肌肉损伤会导致脊髓中谷氨酸释放增加,以及痛觉过敏,而脊髓中NMDA和非NMDA谷氨酸受体的阻断可逆转这种痛觉过敏。因此,我们假设脊髓PKC的激活1)介导肌肉损伤1周后痛觉过敏的晚期阶段,2)通过激活NMDA和非NMDA谷氨酸受体产生机械性痛觉过敏。

结果

给大鼠植入鞘内导管,用于将药物直接输送到脊髓。使用von Frey细丝测定爪的机械性撤针阈值。鞘内注射佛波酯12,13 - 二丁酸酯(PDBu)导致爪的机械性撤针阈值呈剂量依赖性降低,而PKC抑制剂GF109203X预处理可防止这种降低。用NMDA受体拮抗剂(AP5)或AMPA/海人藻酸受体拮抗剂(NBQX)预处理可防止PDBu引起的机械性撤针阈值降低。在腓肠肌中注射两次酸性盐水会使第二次注射后24小时和1周时双侧爪的机械性撤针阈值降低。然而,与载体对照相比,脊髓中PKC的阻断对爪撤针阈值的降低没有影响。

结论

脊髓PKC的激活产生爪的机械性痛觉过敏,这依赖于NMDA和非NMDA受体的激活。另一方面,慢性肌肉诱导的机械性痛觉过敏不利用脊髓PKC。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bd7/1482680/720635a3cef1/1744-8069-2-13-1.jpg

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