Evidence map›Paper›PMID 40392031›Full record

ArticleBiomolecules & biomedicine2025

Cutaneous inflammation alters nociceptor electrophysiology in guinea pigs but not rats.

Laiche Djouhri, Ahmed Eliwa, Alghalya Al-Emadi, Yehia Y Hussein, Hissa Al-Suwaidi, Al-Jouhara Albaloshi, Ayman Mustafa, Mohammed Seed Ahmed

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Article in Biomolecules & biomedicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Laiche DjouhriDepartment of Basic Medical Sciences, College of Medicine, QU Health, Qatar University, Doha, Qatar.
Ahmed EliwaCollege of Medicine, QU Health, Qatar University, Doha, Qatar.
Alghalya Al-EmadiCollege of Medicine, QU Health, Qatar University, Doha, Qatar.
Yehia Y HusseinDepartment of Orthopedic Surgery, Hamad Medical Corporation, Doha, Qatar.
Hissa Al-SuwaidiCollege of Medicine, QU Health, Qatar University, Doha, Qatar.
Al-Jouhara AlbaloshiCollege of Medicine, QU Health, Qatar University, Doha, Qatar.
Ayman MustafaDepartment of Basic Medical Sciences, College of Medicine, QU Health, Qatar University, Doha, Qatar.
Mohammed Seed AhmedDepartment of Basic Medical Sciences, College of Medicine, QU Health, Qatar University, Doha, Qatar.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory pain hypersensitivity is believed to result, in part, from increased excitability of nociceptive dorsal root ganglion (DRG) neurons. We previously demonstrated in guinea pigs that hindlimb inflammation induces electrophysiological changes in these neurons, including faster action potential (AP) and afterhyperpolarization (AHP) kinetics. Given that rats and guinea pigs are distinct species with notable differences in genetic composition and physiology, we hypothesized that cutaneous inflammation would have different effects on the electrophysiological properties of nociceptive DRG neurons in rats-the predominant rodent model for pain research. To test this hypothesis, we performed intracellular voltage recordings from DRG neurons (n = 430) in deeply anesthetized, untreated (control) and complete Freund's adjuvant (CFA)-treated rats and guinea pigs. C-, Aδ-, and Aβ-nociceptors were identified based on their dorsal root conduction velocities (CVs) and responses to natural noxious stimuli. Consistent with our hypothesis, we observed no significant changes in any electrophysiological variables in rat nociceptive neurons four days after CFA-induced hindlimb inflammation. In contrast, guinea pig nociceptors exhibited a significant increase in CV and significant decreases in both AP and AHP durations. The inflammation-induced shortening of absolute and relative refractory periods likely contributes to increased firing frequency in nociceptive nerve fibers, thereby promoting inflammatory pain hypersensitivity. These findings suggest species-specific differences in peripheral neuronal mechanisms underlying inflammatory pain, potentially due to variation in ion channel expression and/or function in DRG neurons between rats and guinea pigs. Given the genetic and metabolic similarities between guinea pigs and humans, further research is warranted to determine whether guinea pigs may serve as a more accurate model of chronic inflammatory pain than rats.

Indexed as

InflammationNociceptorsSkinAction PotentialsAnimalsFreund's AdjuvantGanglia, SpinalGuinea PigsMaleRatsRats, Sprague-DawleyFreund's Adjuvant

Identifiers

PMID40392031
PMCPMC12452121

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.