Inhibiting astrocytic activation: a novel analgesic mechanism of ketamine at the spinal level?

J Neurochem. 2009 Jun;109(6):1691-700. doi: 10.1111/j.1471-4159.2009.06087.x. Epub 2009 Apr 4.

Abstract

Although ketamine is widely used as an analgesic agent and has an anti-allodynic effect on neuropathic pain, the underlying analgesic mechanisms are not fully explained by the modern 'neuronal-based' theories. As emerging studies have focused on the critical role of spinal astrocytes in the pathological pain states, we have hypothesized that there exist some 'astrocytes-related' mechanisms in the analgesic function of ketamine. In the present study, using the spinal nerve ligation (SNL) pain model, we investigated the anti-nociceptive effects of intraperitoneal or intrathecal ketamine on SNL-induced neuropathic pain response, meanwhile, we investigated the astrocytic activation after ketamine administration on SNL rats. Behavioral data showed that either intraperitoneal or intrathecal ketamine inhibited SNL-induced allodynia, however, immunohistochemistry showed that SNL induced astrocytic activation was suppressed by intrathecal but not intraperitoneal ketamine. Using quantitative Western blot analysis, our report showed that intrathecal ketamine down-regulated glial fibrillary acidic protein expression, suggesting inhibition of SNL-induced astrocytic activation, which wasn't influenced by intraperitoneal administration. We conclude that intraperitoneal ketamine could alleviate SNL-induced neuropathic pain via the classical 'neuronal-based' mechanisms, but in addition, 'astrocytes-related' mechanisms were also important underlying the anti-allodynic effect of intrathecal ketamine.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Analgesics / pharmacology*
  • Anesthesia*
  • Animals
  • Astrocytes / drug effects*
  • Disease Models, Animal
  • Drug Administration Routes
  • Glial Fibrillary Acidic Protein / metabolism
  • Ketamine / pharmacology*
  • Ligation / methods
  • Male
  • Pain / etiology*
  • Pain Measurement
  • Pain Threshold / drug effects
  • Pain Threshold / physiology
  • Rats
  • Rats, Sprague-Dawley
  • Reaction Time / drug effects
  • Spinal Cord Injuries / complications*
  • Time Factors
  • Up-Regulation / drug effects

Substances

  • Analgesics
  • Glial Fibrillary Acidic Protein
  • Ketamine