Source Paper
Activated Microglia Contribute to the Maintenance of Chronic Pain after Spinal Cord Injury
Bryan C. Hains, Stephen G. Waxman
Journal of Neuroscience • 2006
Spinal Cord Contusion Injury
Objective: To test the hypothesis that activated microglia contribute to chronic pain after spinal cord injury by inducing T9 spinal cord contusion injury and evaluating the effects of microglial inhibition on pain-related behaviors and neuronal hyperresponsiveness
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Protocol Steps
Spinal cord contusion injury induction
Adult male Sprague Dawley rats underwent T9 spinal cord contusion injury to model traumatic spinal cord injury
Note: Injury performed at thoracic level 9 (T9)
View evidence from paper
“adult male Sprague Dawley rats underwent T9 spinal cord contusion injury”
Post-injury observation period
Animals were observed for four weeks after injury to allow development of chronic pain phenotype and microglial activation
Note: At this timepoint, lumbar dorsal horn neurons became hyperresponsive and behavioral nociceptive thresholds were decreased
View evidence from paper
“Four weeks after injury, when lumbar dorsal horn multireceptive neurons became hyperresponsive and when behavioral nociceptive thresholds were decreased to both mechanical and thermal stimuli”
Baseline behavioral assessment
Measurement of nociceptive thresholds to mechanical and thermal stimuli before minocycline treatment initiation
Note: Establishes baseline pain-related behavior at 4 weeks post-injury
View evidence from paper
“behavioral nociceptive thresholds were decreased to both mechanical and thermal stimuli”
Intrathecal minocycline infusion initiation
Intrathecal infusions of minocycline microglial inhibitor were initiated at four weeks post-injury
Touch Screen Constant Laboratory Syringe Pump
Matches: Intrathecal infusion pump/delivery system
Note: Delivery method and dosage not specified in provided text
View evidence from paper
“intrathecal infusions of the microglial inhibitor minocycline were initiated”
Electrophysiological recording during minocycline treatment
Electrophysiological experiments conducted to measure lumbar dorsal horn neuronal responses during minocycline administration
Note: Minocycline rapidly attenuated hyperresponsiveness of lumbar dorsal horn neurons
View evidence from paper
“Electrophysiological experiments showed that minocycline rapidly attenuated hyperresponsiveness of lumbar dorsal horn neurons”
Behavioral assessment during minocycline treatment
Measurement of nociceptive thresholds to mechanical and thermal stimuli during minocycline infusion
Note: Minocycline restored nociceptive thresholds to normal levels
View evidence from paper
“Behavioral data showed that minocycline restored nociceptive thresholds”
Microglial morphology assessment
Examination of spinal microglial cell morphology during minocycline treatment
Note: Microglial cells assumed a quiescent morphological phenotype during minocycline treatment
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“spinal microglial cells assumed a quiescent morphological phenotype”
Phosphorylated-p38 level measurement
Measurement of phosphorylated-p38 protein levels in spinal cord tissue during minocycline treatment
Note: Levels of phosphorylated-p38 were decreased in SCI animals receiving minocycline
View evidence from paper
“Levels of phosphorylated-p38 were decreased in SCI animals receiving minocycline”
Minocycline delivery cessation
Discontinuation of minocycline intrathecal infusion to assess reversibility of treatment effects
Touch Screen Constant Laboratory Syringe Pump
Matches: Intrathecal infusion pump/delivery system
Note: Cessation resulted in immediate return of pain-related phenomena
View evidence from paper
“Cessation of delivery of minocycline resulted in an immediate return of pain-related phenomena”