Gabapentin reverses central hypersensitivity and suppresses medial prefrontal cortical glucose metabolism in rats with neuropathic pain View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2014-12

AUTHORS

Hsiao-Chun Lin, Yu-Hsin Huang, Tzu-Hao Harry Chao, Wen-Ying Lin, Wei-Zen Sun, Chen-Tung Yen

ABSTRACT

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. More... »

PAGES

63

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/1744-8069-10-63

DOI

http://dx.doi.org/10.1186/1744-8069-10-63

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1009946501

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/25253440


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