Journal
MOLECULAR PAIN
Volume 10, Issue -, Pages -Publisher
SAGE PUBLICATIONS INC
DOI: 10.1186/1744-8069-10-63
Keywords
Gabapentin; Allodynia; FDG-PET; Functional connectivity; Neuropathic pain
Categories
Funding
- National Science Council, Taiwan [NSC100-2311-B002-002-MY3, 100-2321-B-002-079]
- National Taiwan University Hospital, Taiwan [UN102-023]
- National Health Research Institutes, Taiwan [NHRI-EX102-10104NI]
Ask authors/readers for more resources
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 F-18-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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available