Pain Sensitivity Measurement
Objective: Assessed pain sensitivity in transgenic mice overexpressing COMT-Val and COMT-null mutant mice to determine the role of COMT gene in pain sensitivity and stress responses
This is a Pain Sensitivity Measurement protocol using mouse as the model organism. The procedure involves 1 procedural steps. Extracted from a 2008 paper published in Journal of Neuroscience.
Model and subjects
mouse • transgenic mice overexpressing human COMT-Val polymorphism (Val-tg) and COMT-null mutant mice • unknown • not specified • not specified
Study window
Estimated timing pending
Core workflow
Pain Sensitivity Assessment
Primary readouts
- Pain sensitivity levels in Val-tg mice versus wild-type controls
- Pain sensitivity levels in COMT-null mutant mice versus wild-type controls
- Correlation between COMT enzyme activity and pain sensitivity
Key equipment and reagents
Verified items
0
Direct vendor links
0
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Protocol Steps
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Pain Sensitivity Assessment
Pain sensitivity was assessed in transgenic mice overexpressing COMT-Val and COMT-null mutant mice. The study found that increased COMT enzyme activity in Val-tg mice resulted in blunted pain sensitivity, while COMT disruption increased pain sensitivity.
Note: Specific pain sensitivity testing methodology (e.g., hot plate test, tail flick test, von Frey filaments) is not detailed in the provided text
View evidence from paper
“Increased COMT enzyme activity in Val-tg mice resulted in disrupted attentional set-shifting abilities, and impaired working and recognition memory, but blunted stress responses and pain sensitivity. Conversely, COMT disruption improved working memory, but increased stress responses and pain sensitivity.”