Literature DB >> 31323014

Sham surgeries for central and peripheral neural injuries persistently enhance pain-avoidance behavior as revealed by an operant conflict test.

Max A Odem1, Michael J Lacagnina2, Stephen L Katzen1, Jiahe Li2, Emily A Spence1, Peter M Grace2, Edgar T Walters1.   

Abstract

Studies using rodent models of neuropathic pain use sham surgery control procedures that cause deep tissue damage. Sham surgeries would thus be expected to induce potentially long-lasting postsurgical pain, but little evidence for such pain has been reported. Operant tests of voluntary behavior can reveal negative motivational and cognitive aspects of pain that may provide sensitive tools for detecting pain-related alterations. In a previously described operant mechanical conflict test involving lengthy familiarization and training, rodents freely choose to either escape from a brightly lit chamber by crossing sharp probes or refuse to cross. Here, we describe a brief (2-day) mechanical conflict protocol that exploits rats' innate exploratory response to a novel environment to detect persistently enhanced pain-avoidance behavior after sham surgeries for 2 neural injury models: thoracic spinal cord injury and chronic constriction injury of the sciatic nerve. Pitting the combined motivations to avoid the bright light and to explore the novel device against pain from crossing noxious probes disclosed a conflicting, hyperalgesia-related reluctance to repeatedly cross the probes after injury. Rats receiving standard sham surgeries demonstrated enhanced pain-like avoidance behavior compared with naive controls, and this behavior was similar to that of corresponding chronic constriction injury or spinal cord injury rats weeks or months after injury. In the case of sham surgery for spinal cord injury, video analysis of voluntary exploratory behavior directed at the probes revealed enhanced forepaw withdrawal responses. These findings have important implications for preclinical investigations into behavioral alterations and physiological mechanisms associated with postsurgical and neuropathic pain.

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Year:  2019        PMID: 31323014      PMCID: PMC6800634          DOI: 10.1097/j.pain.0000000000001642

Source DB:  PubMed          Journal:  Pain        ISSN: 0304-3959            Impact factor:   7.926


  95 in total

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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.

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Review 4.  Predictive validity of behavioural animal models for chronic pain.

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6.  Painful nerve injury upregulates thrombospondin-4 expression in dorsal root ganglia.

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Authors:  Megan Ryan Detloff; Rodel E Wade; John D Houlé
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Review 10.  Neuronal-Glial Interactions Maintain Chronic Neuropathic Pain after Spinal Cord Injury.

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  10 in total

1.  Comprehensive Preclinical Assessment of Sensory, Functional, Motivational-Affective, and Neurochemical Outcomes in Neuropathic Pain: The Case of the Sigma-1 Receptor.

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2.  Macrophage Migration Inhibitory Factor (MIF) Makes Complex Contributions to Pain-Related Hyperactivity of Nociceptors after Spinal Cord Injury.

Authors:  Alexis G Bavencoffe; Emily A Spence; Michael Y Zhu; Anibal Garza-Carbajal; Kerry E Chu; Ona E Bloom; Carmen W Dessauer; Edgar T Walters
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3.  Comprehensive phenotyping of cutaneous afferents reveals early-onset alterations in nociceptor response properties, release of CGRP, and hindpaw edema following spinal cord injury.

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4.  Duration of Reduction in Enduring Stress-Induced Hyperalgesia Via FKBP51 Inhibition Depends on Timing of Administration Relative to Traumatic Stress Exposure.

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5.  Mechanical Conflict-Avoidance Assay to Measure Pain Behavior in Mice.

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6.  Adaptive mechanisms driving maladaptive pain: how chronic ongoing activity in primary nociceptors can enhance evolutionary fitness after severe injury.

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7.  Sex-specific transcriptome of spinal microglia in neuropathic pain due to peripheral nerve injury.

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8.  Transcriptional Profiling of Non-injured Nociceptors After Spinal Cord Injury Reveals Diverse Molecular Changes.

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9.  Small molecule targeting NaV1.7 via inhibition of the CRMP2-Ubc9 interaction reduces pain in chronic constriction injury (CCI) rats.

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10.  EPAC1 and EPAC2 promote nociceptor hyperactivity associated with chronic pain after spinal cord injury.

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  10 in total

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