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Quantitative assessment of tactile allodynia in the rat paw
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Chronic catheterization of the spinal subarachnoid space
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Antinociceptive actions of spinal nonsteroidal anti-inflammatory agents on the formalin test in the rat.
TLDR
These studies indicate that NSAID have a powerful effect upon spinal nociceptive processing evoked by the s.c.p.t. injection of formalin.
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Behavioral and autonomic correlates of the tactile evoked allodynia produced by spinal glycine inhibition: effects of modulatory receptor systems and excitatory amino acid antagonists
  • T. Yaksh
  • Biology, Psychology
    Pain
  • 1 April 1989
View on Elsevier
Activation of p38 mitogen‐activated protein kinase in spinal microglia is a critical link in inflammation‐induced spinal pain processing
TLDR
Results indicate that spinal p38 MAPK is involved in inflammation‐induced pain and that activated spinal microglia play a direct role in spinal nociceptive processing.
View on Wiley
Intrathecal minocycline attenuates peripheral inflammation‐induced hyperalgesia by inhibiting p38 MAPK in spinal microglia
TLDR
Findings show that minocycline given IT produces a potent and consistent antinociception in models of tissue injury and inflammation‐evoked pain, and they provide strong support for the idea that this effect is mediated by direct inhibition of spinal microglia and subsequent activation of p38 in these cells.
View on Wiley
Efficacy of spinal NMDA receptor antagonism in formalin hyperalgesia and nerve injury evoked allodynia in the rat.
TLDR
NMDA antagonists by the spinal route appear to be useful therapeutic agents for chemically induced facilitated pain as well as nerve injury induced tactile allodynia.
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Hyperalgesia mediated by spinal glutamate or substance P receptor blocked by spinal cyclooxygenase inhibition.
TLDR
These findings demonstrate that the analgesic effects of NSAIDs can be dissociated from their anti-inflammatory actions, and are thus critical for the augmented processing of pain information at the spinal level.
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Increased Sensitivity of Injured and Adjacent Uninjured Rat Primary Sensory Neurons to Exogenous Tumor Necrosis Factor-α after Spinal Nerve Ligation
TLDR
It is concluded that injured and adjacent uninjured DRG neurons are sensitized to TNF after SNL, suggesting that Sensitization to endogenous TNF may be essential for the development and maintenance of neuropathic pain.
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Upregulation of Dorsal Root Ganglion α2δ Calcium Channel Subunit and Its Correlation with Allodynia in Spinal Nerve-Injured Rats
TLDR
Using a rat neuropathic pain model in which gabapentin-sensitive tactile allodynia develops after tight ligation of the left fifth and sixth lumbar spinal nerves, a >17-fold, time-dependent increase in α2δ subunit expression in DRGs ipsilateral to the nerve injury is found, suggesting that DRG α2 δ regulation may play an unique role in neuroplasticity after peripheral nerve injury.
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