Lin Hsiao-Chun, Huang Yu-Hsin, Chao Tzu-Hao Harry, Lin Wen-Ying, Sun Wei-Zen, Yen Chen-Tung
Department of Life Science, National Taiwan University, No 1, Section 4, Roosevelt Road, Taipei 10617, Taiwan.
Mol Pain. 2014 Sep 25;10:63. doi: 10.1186/1744-8069-10-63.
Gabapentin (GBP) is known to suppress neuropathic hypersensitivity of primary afferents and the spinal cord dorsal horn. However, its supra-spinal action sites are unclear. We identify the brain regions where GBP changes the brain glucose metabolic rate at the effective dose that alleviates mechanical allodynia using 18 F-fluorodeoxyglucose-positron emission tomography (FDG-PET) scanning.
Comparing the PET imaging data before and after the GBP treatment, the spared nerve injury-induced increases of glucose metabolism in the thalamus and cerebellar vermis were reversed, and a significant decrease occurred in glucose metabolism in the medial prefrontal cortex (mPFC), including the anterior cingulate cortex. GBP treatment also reversed post-SNI connectivity increases between limbic cortices and thalamus.
Our results indicate that GBP analgesic effect may be mediated by reversing central hypersensitivity, and suppressing mPFC, a crucial part of the cortical representation of pain, in the brain.
已知加巴喷丁（GBP）可抑制初级传入神经和脊髓背角的神经性超敏反应。然而，其脊髓上的作用位点尚不清楚。我们使用18F-氟脱氧葡萄糖-正电子发射断层扫描（FDG-PET）扫描，确定在减轻机械性异常性疼痛的有效剂量下，GBP改变脑葡萄糖代谢率的脑区。
比较GBP治疗前后的PET成像数据， spared神经损伤诱导的丘脑和小脑蚓部葡萄糖代谢增加得到逆转，内侧前额叶皮质（mPFC），包括前扣带回皮质的葡萄糖代谢显著降低。GBP治疗还逆转了SNI后边缘皮质和丘脑之间的连接性增加。
我们的结果表明，GBP的镇痛作用可能是通过逆转中枢超敏反应，并抑制大脑中疼痛皮质表征的关键部分mPFC来介导的。
