Tumor implantation in mouse humerus evokes movement-related hyperalgesia exceeding that evoked by intramuscular carrageenan

  title={Tumor implantation in mouse humerus evokes movement-related hyperalgesia exceeding that evoked by intramuscular carrageenan},
  author={P. W. Wacnik and Lois J. Kehl and Thomas M. Trempe and Margaret L. R. Ramnaraine and Alvin J. Beitz and George L. Wilcox},

Tumor-evoked sensitization of C nociceptors: a role for endothelin.

It is concluded that ET-1 at the tumor site contributes to tumor-evoked excitation and sensitization of C nociceptors through an ETA receptor mediated mechanism.

Changes in response properties of nociceptive dorsal horn neurons in a murine model of cancer pain.

It is shown that sensitization of WDR neurons, but not HT neurons, contributes to tumor-evoked hyperalgesia, which is often severe and debilitating when cancer metastasizes to bone.

Intrathecal urocortin I in the spinal cord as a murine model of stress hormone‐induced musculoskeletal and tactile hyperalgesia

Data indicate that urocortin I acts at CRF receptors in the mouse spinal cord to elicit a reproducible and persistent tactile and musculoskeletal hyperalgesia, which may serve as a screen for drugs that alleviate painful conditions that are exacerbated by stress.

Cancer pain physiology

Treatments for cancer pain are described in terms of mechanistic insights and in the case of opioids, which modulate pain transmission at spinal and supraspinal sites, their use can be compromised by opioid-induced hyperalgesia.

A Decrease in Anandamide Signaling Contributes to the Maintenance of Cutaneous Mechanical Hyperalgesia in a Model of Bone Cancer Pain

Evidence is provided that manipulation of peripheral endocannabinoid signaling is a promising strategy for the management of bone cancer pain by suppressing the anti-hyperalgesic effect of elevated AEA levels.



A new animal model for assessing mechanisms and management of muscle hyperalgesia

Functional Interactions between Tumor and Peripheral Nerve: Morphology, Algogen Identification, and Behavioral Characterization of a New Murine Model of Cancer Pain

A model of tumor-induced bone destruction and hyperalgesia produced by implantation of fibrosarcoma cells into the mouse calcaneus bone provides a unique approach for quantifying the behavioral, biochemical, and electrophysiological consequences of tumor–nerve interactions.

A rat model of bone cancer pain

Neurochemical and Cellular Reorganization of the Spinal Cord in a Murine Model of Bone Cancer Pain

The alterations in the neurochemistry of the spinal cord and the sensitization of primary afferents were positively correlated with the extent of bone destruction and the growth of the tumor and appears unique when compared to changes that occur in persistent inflammatory or neuropathic pain states.

Functional interactions between tumor and peripheral nerve: changes in excitability and morphology of primary afferent fibers in a murine model of cancer pain.

  • D. CainP. Wacnik D. Simone
  • Biology
    The Journal of neuroscience : the official journal of the Society for Neuroscience
  • 2001
The development of spontaneous activity and sensitization to heat in C-fibers and increased innervation of cutaneous structures within the first 2 weeks of tumor growth suggest activation and sensitizing of a proportion of C-Fibers in this model of cancer pain.

Localized, tumor‐associated osteolysis involves the recruitment and activation of osteoclasts

Findings define a model that is useful for the study of tumor osteolysis, and the data from analyses of the model demonstrate that the cellular mechanisms responsible for 2472 tumor‐induced osteolytic activity include both an increase in the number of osteoclasts and activation of mature osteoclast.

Transplants of Adrenal Medullary Chromaffin Cells Reduce Forelimb and Hindlimb Allodynia in a Rodent Model of Chronic Central Pain after Spinal Cord Hemisection Injury

The therapeutic potential of transplanted adrenal medullary chromaffin cells, which secrete catecholamines and opioid peptides near the spinal cord, is supported in reducing chronic central pain following spinal cord injury.

Osteoprotegerin blocks bone cancer-induced skeletal destruction, skeletal pain and pain-related neurochemical reorganization of the spinal cord

It is demonstrated that excessive tumor-induced bone destruction is involved in the generation of bone cancer pain and that osteoprotegerin may provide an effective treatment for this common human condition.