Gabapentin potentiates N-methyl-D-aspartate receptor mediated currents in rat GABAergic dorsal horn neurons

Research output: Contribution to journalArticle

33 Scopus citations


We previously reported that gabapentin (GBP), a widely prescribed analgesic, enhances N-methyl-D-aspartate (NMDA) receptor mediated currents only when the intracellular level of protein kinase C is elevated. However, it is unclear how the potentiation of NMDA responses by GBP can lead to pain relief. To resolve this issue, we combined immunocytochemical and patch recording techniques to study the actions of GBP on NMDA receptors in dorsal horn cells isolated from rats with inflammation and to determine the gamma-aminobutyric acid (GABA) content in the recorded cells. We found that all GBP-responsive cells are GABA-immunoreactive and none of the GABA-negative neurons respond to GBP. Thus, GBP appears to enhance NMDA currents in GABAergic neurons. These observations suggest that GBP exerts its antinociceptive action by increasing the activity of these inhibitory neurons.

Original languageEnglish (US)
Pages (from-to)177-180
Number of pages4
JournalNeuroscience Letters
Issue number3
StatePublished - May 24 2002



  • Gabapentin
  • Gamma-aminobutyric acid immunoreactivity
  • N-methyl-D-aspartate
  • Perforated patch clamp
  • Protein kinase C
  • Spinal cord

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this