Conditioned Place Aversion
Objective: Measurement of place aversion induced by CRF, urocortin III, or KOR agonist injection to assess dysphoric component of stress encoded by dynorphin κ-opioid system
This is a Conditioned Place Aversion protocol using mouse as the model organism. The procedure involves 4 procedural steps, 1 equipment items, 7 materials. Extracted from a 2008 paper published in Journal of Neuroscience.
Model and subjects
mouse • Not specified in provided text • unknown • Not specified in provided text • Not specified in provided text
Study window
Estimated timing pending
Core workflow
Drug injection and place aversion testing • Antagonist administration • Genetic manipulation comparison
Primary readouts
- Place aversion behavior induced by CRF injection
- Place aversion behavior induced by urocortin III injection
- Place aversion behavior induced by KOR agonist U50,488
- Blockade of place aversion by KOR antagonist
Key equipment and reagents
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Protocol Steps
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Drug injection and place aversion testing
Mice received injections of CRF, urocortin III, or KOR agonist U50,488 and were tested for place aversion behavior
Note: Place aversion was measured as the primary outcome
View evidence from paper
“Injection of corticotropin-releasing factor (CRF) or urocortin III, key mediators of the stress response, produced place aversion”
Antagonist administration
KOR antagonist, CRF2 receptor antagonist (antisauvigine-30), or CRF1 receptor antagonist (antalarmin) were administered to block place aversion
Note: Different antagonists were tested to determine receptor specificity
View evidence from paper
“CRF-induced place aversion was blocked by the CRF 2 receptor antagonist antisauvigine-30, but not by the CRF 1 receptor antagonist antalarmin”
Genetic manipulation comparison
Place aversion responses were compared between wild-type mice and mice lacking dynorphin gene
Note: Dynorphin knockout mice showed absent aversive behaviors
View evidence from paper
“aversive behaviors that were blocked by a κ-opioid receptor (KOR) antagonist and absent in mice lacking dynorphin”
Brain imaging of KOR activation
Phospho-selective antibody directed against activated KOR was used to image sites of dynorphin action in brain regions
Note: Imaging revealed KOR activation in basolateral amygdala, nucleus accumbens, dorsal raphe, and hippocampus
View evidence from paper
“stress and CRF each caused dynorphin-dependent KOR activation in the basolateral amygdala, nucleus accumbens, dorsal raphe, and hippocampus”