期刊论文详细信息
Molecular Pain
Gabapentin reverses central hypersensitivity and suppresses medial prefrontal cortical glucose metabolism in rats with neuropathic pain
Chen-Tung Yen2  Wei-Zen Sun1  Wen-Ying Lin1  Tzu-Hao Harry Chao2  Yu-Hsin Huang1  Hsiao-Chun Lin2 
[1] Department of Anesthesiology, National Taiwan University Hospital, Taipei 10002, Taiwan;Department of Life Science, National Taiwan University, No 1, Section 4, Roosevelt Road, Taipei 10617, Taiwan
关键词: Neuropathic pain;    Functional connectivity;    FDG-PET;    Allodynia;    Gabapentin;   
Others  :  1161771
DOI  :  10.1186/1744-8069-10-63
 received in 2014-04-03, accepted in 2014-09-10,  发布年份 2014
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【 摘 要 】

Background

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.

Results

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.

Conclusions

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.

【 授权许可】

   
2014 Lin et al.; licensee BioMed Central Ltd.

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