Bone Cancer Pain Model
Objective: Measure ongoing and movement-evoked nocifensive behaviors in an in vivo model of bone cancer pain in mice to evaluate TRPV1 antagonist efficacy
Gather these items before starting the experiment. Check off items as you prepare.
Equipment1
Not applicable • Not applicable • Not applicable • Not specified
Materials1
Johnson and Johnson Pharmaceutical Research and Development • Not specified • Not specified • Not specified
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Protocol Steps
Establish bone cancer pain model
Induce bone cancer colonization in mouse femur to activate osteoclasts and produce local tissue acidosis and bone resorption
Note: This process generates both ongoing and movement-evoked pain through nociceptor activation
View evidence from paper
“Cancer colonization of bone leads to the activation of osteoclasts, thereby producing local tissue acidosis and bone resorption”
Administer TRPV1 antagonist
Administer TRPV1 antagonist either acutely or chronically to test pain attenuation
Note: Antagonist showed similar efficacy in reducing early, moderate, and severe pain-related responses
View evidence from paper
“acute or chronic administration of a TRPV1 antagonist or disruption of the TRPV1 gene results in a significant attenuation of both ongoing and movement-evoked nocifensive behaviors”
Measure ongoing nocifensive behaviors
Assess spontaneous pain-related behaviors in mice with bone cancer
Note: Ongoing behaviors reflect spontaneous pain generation from tissue acidosis and bone resorption
View evidence from paper
“in an in vivo model of bone cancer pain, acute or chronic administration of a TRPV1 antagonist results in a significant attenuation of both ongoing and movement-evoked nocifensive behaviors”
Measure movement-evoked nocifensive behaviors
Assess pain-related behaviors triggered by movement or weight-bearing in mice with bone cancer
Note: Movement-evoked behaviors reflect pain triggered by mechanical stimulation during normal activity
View evidence from paper
“in an in vivo model of bone cancer pain, acute or chronic administration of a TRPV1 antagonist results in a significant attenuation of both ongoing and movement-evoked nocifensive behaviors”
Use TRPV1 gene disruption model
Compare results with mice lacking functional TRPV1 gene to confirm receptor involvement
Note: Gene disruption provides genetic validation of pharmacological antagonist findings
View evidence from paper
“acute or chronic administration of a TRPV1 antagonist or disruption of the TRPV1 gene results in a significant attenuation of both ongoing and movement-evoked nocifensive behaviors”