Emotion circuits
Where does nociplastic pain hitch a ride in the amygdala?
Open access · cc by · source: Europe PMC
In TRAP2 mice, inflammation-tagged parabrachial (elPB) neurons project most densely to posterior capsular central amygdala (pCeC) and form strong synapses with pain-tagged pCeC cells; exciting those CeA neurons recreates bilateral hindpaw sensitization.
Study at a glance
- Design
- Animal / in-vitro — fosTRAP2 mouse circuit study of nociplastic pain: activity-dependent tagging, optogenetics, and chemogenetics of elPB–CeA neurons after transient inflammation
- N
- N=9 · Multiple TRAP2 experiments; slice physiology example TRAPed n=39 cells from M=9 mice; tracing/chemogenetics used additional animals
- Population
- Transgenic TRAP2 (fosTRAP2) mice after transient localized (upper-lip) inflammation
- Outcome
- Whether pain-tagged elPB neurons synaptically co-activate posterior capsular CeA (pCeC) neurons that drive nociplastic sensitization
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Key findings
NociTRAPed elPB neurons projected widely but most densely to CeA, especially caudal capsular CeA (pCeC, about −1.4 to −1.9 mm from bregma), with robust synapses onto nociTRAPed pCeC neurons. Exciting nociTRAPed CeA neurons reproduced bilateral hindpaw sensitization without ongoing nociceptor drive.
Methodology
After transient localized inflammation, they used fosTRAP2 mice to express ChR2-YFP, markers, and DREADDs in pain-activated neurons, then mapped elPB projections, recorded pCeC synapses, and chemogenetically/optogenetically tested behavior.
Limitations
Mouse lip-inflammation TRAP does not prove this circuit is the sole cause of human fibromyalgia-type nociplastic pain, and tagging is activity-history based, not a complete cell-type census.
How this study connects
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