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CENTRAL AMYGDALA PKCΔ AND TRPA1 MOLECULAR PROFILING IN A RAT MODEL OF CHRONIC NEUROPATHIC PAIN
Marie Soukupovaand 6 co-authors
University of Ferrara
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS07-10AM-627
Presentation
Date TBA
Board: PS07-10AM-627
Event Information
Poster Board
PS07-10AM-627
Poster
View posterAbstract
Chronic neuropathic pain involves persistent mechanical hypersensitivity and significant affective-emotional remodeling. The central amygdala (CeA) is a critical limbic node for the affective-motivational processing of pain. This study investigated molecular adaptations within the CeA following peripheral nerve injury, specifically focusing on protein kinase C delta (PKCδ) and the Transient Receptor Potential Ankyrin 1 (TRPA1) ion channel.
Chronic neuropathy was induced in male and female Wistar rats via partial sciatic nerve ligation (pSNL). Mechanical allodynia was monitored for 21 days post-ligation using von Frey filaments. CeA tissues from pSNL and sham-operated groups were analyzed using in situ hybridization (RNAscope) and Western blot to quantify PKCδ and TRPA1 mRNA and protein expression.
Behavioral assessments confirmed mechanical allodynia in both sexes following pSNL, though the threshold was lower in females compared to males. Molecular analysis revealed discrete alterations in the expression patterns of PKCδ and TRPA1 within the CeA of nerve-injured animals compared to sham controls.
Overall, this study provides preliminary evidence that PKCδ and TRPA1 in the CeA are integral components of the central signalling pathways responding to neuropathic injury.
Chronic neuropathy was induced in male and female Wistar rats via partial sciatic nerve ligation (pSNL). Mechanical allodynia was monitored for 21 days post-ligation using von Frey filaments. CeA tissues from pSNL and sham-operated groups were analyzed using in situ hybridization (RNAscope) and Western blot to quantify PKCδ and TRPA1 mRNA and protein expression.
Behavioral assessments confirmed mechanical allodynia in both sexes following pSNL, though the threshold was lower in females compared to males. Molecular analysis revealed discrete alterations in the expression patterns of PKCδ and TRPA1 within the CeA of nerve-injured animals compared to sham controls.
Overall, this study provides preliminary evidence that PKCδ and TRPA1 in the CeA are integral components of the central signalling pathways responding to neuropathic injury.
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