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1.  Validity of acute and chronic tactile sensory testing after spinal cord injury in rats 
Experimental neurology  2010;225(2):366-376.
Spinal cord injury (SCI) impairs sensory systems causing allodynia. Measuring the development of allodynia in rodent models of SCI is challenging due to spinal shock and marked motor impairments. Assessment of SCI-induced allodynia is not standardized across labs, making interpretation of results difficult. Therefore, we validated sensory threshold assessment after SCI and developed a novel assessment of allodynia prior to motor recovery in a rat SCI model. One hundred fifty-six Sprague–Dawley rats received T8 laminectomy or mild to moderate SCI using the OSU SCI device (0.3 mm to 1.3mm cord displacement). To determine tactile thresholds, von Frey hairs (VFH) were applied in Up–Down or ascending order to the dorsal or plantar hindpaw. The most efficient and valid procedures that maintain high sensitivity and specificity were identified. Ten Up–Down VFH applications yielded stable thresholds; reducing the risk of threshold decay and unnecessary exposure to painful stimuli. Importantly, distraction of SCI-rats with food revealed differential decay of thresholds than when distraction is not provided. The new test uses dorsal VFH stimulation and is independent of trunk or hindlimb control. Acute dorsal VFH thresholds collected before recovery of hindlimb weight support accurately predicted plantar VFH thresholds measured at late timepoints (χ2=8.479; p<0.05). Thus, standardized testing early after SCI using the dorsal VFH test or later using 10 stimuli in the Up–Down test produces valid measures of tactile sensation across many SCI severities. Early detection of allodynia in experimental SCI will allow identification of mechanisms responsible for pain development and determine targets for therapeutic interventions.
PMCID: PMC4933012  PMID: 20643128
von Frey Hair; Allodynia; Rats; Withdrawal threshold; Distraction
2.  Remote activation of microglia and pro-inflammatory cytokines predict the onset and severity of below-level neuropathic pain after spinal cord injury in rats 
Experimental neurology  2008;212(2):337-347.
Spinal cord injury (SCI) impairs sensory systems causing chronic allodynia. Mechanisms underlying neuropathic pain have been more extensively studied following peripheral nerve injury than after central trauma. Microglial activation, pro-inflammatory cytokine production and activation of p38 MAP kinase pathways may induce at-level allodynia following PNI. We investigated whether midthoracic SCI elicits similar behavioral and cellular responses below the level of injury (lumbar spinal cord; L5). Importantly, we show that anatomical connections between L5 and supraspinal centers remain intact after moderate SCI allowing direct comparison to a well-established model of peripheral nerve injury. We found that SCI elicits below-level allodynia of similar magnitude to at-level pain caused by a peripheral nerve injury. Moreover, the presence of robust microglial activation in L5 cord predicted allodynia in 86% of rats. Also increased phosphorylation of p38 MAP kinase occurred in the L5 dorsal horn of allodynic rats. For below-level allodynia after SCI, TNF-α and IL-1β increased in the L5 dorsal horn by 7 dpo and returned to baseline by 35 dpo. Interestingly, IL-6 remains at normal levels early after SCI and increases at chronic time points. Increased levels of pro-inflammatory cytokines also occurred in the thalamus after SCI-induced allodynia. These data suggest that remote microglial activation is pivotal in the development and maintenance of below-level allodynia after SCI. Fractalkine, a known activator of microglia, and astrocytes were not primary modulators of below-level pain. Although the mechanisms of remote microglial activation are unknown, this response may be a viable target for limiting or preventing neuropathic pain after SCI in humans.
PMCID: PMC2600773  PMID: 18511041
allodynia; p38; fractalkine; astrocytes; peripheral nerve injury

Results 1-2 (2)