PMID- 37325677
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230619
IS  - 2673-561X (Electronic)
IS  - 2673-561X (Print)
IS  - 2673-561X (Linking)
VI  - 4
DP  - 2023
TI  - Intraganglionic reactive oxygen species mediate inflammatory pain and 
      hyperalgesia through TRPA1 in the rat.
PG  - 1204057
LID - 10.3389/fpain.2023.1204057 [doi]
LID - 1204057
AB  - Reactive oxygen species (ROS) are generated in nociceptive pathways in response 
      to inflammation and injury. ROS are accumulated within the sensory ganglia 
      following peripheral inflammation, but the functional role of intraganlionic ROS 
      in inflammatory pain is not clearly understood. The aims of this study were to 
      investigate whether peripheral inflammation leads to prolonged ROS accumulation 
      within the trigeminal ganglia (TG), whether intraganglionic ROS mediate pain 
      hypersensitivity via activation of TRPA1, and whether TRPA1 expression is 
      upregulated in TG during inflammatory conditions by ROS. We demonstrated that 
      peripheral inflammation causes excess ROS production within TG during the period 
      when inflammatory mechanical hyperalgesia is most prominent. Additionally, 
      scavenging intraganglionic ROS attenuated inflammatory mechanical hyperalgesia 
      and a pharmacological blockade of TRPA1 localized within TG also mitigated 
      inflammatory mechanical hyperalgesia. Interestingly, exogenous administration of 
      ROS into TG elicited mechanical hyperalgesia and spontaneous pain-like responses 
      via TRPA1, and intraganglionic ROS induced TRPA1 upregulation in TG. These 
      results collectively suggest that ROS accumulation in TG during peripheral 
      inflammation contributes to pain and hyperalgesia in a TRPA1 dependent manner, 
      and that ROS further exacerbate pathological pain responses by upregulating TRPA1 
      expression. Therefore, any conditions that exacerbate ROS accumulation within 
      somatic sensory ganglia can aggravate pain responses and treatments reducing 
      ganglionic ROS may help alleviate inflammatory pain.
CI  - (c) 2023 Zhang, Asgar, Shou, Pak, Da Silva and Ro.
FAU - Zhang, Youping
AU  - Zhang Y
AD  - Department of Neural and Pain Sciences, University of Maryland School of 
      Dentistry, Baltimore, MD, United States.
FAU - Asgar, Jamila
AU  - Asgar J
AD  - Department of Neural and Pain Sciences, University of Maryland School of 
      Dentistry, Baltimore, MD, United States.
FAU - Shou, Huizhong
AU  - Shou H
AD  - Department of Neural and Pain Sciences, University of Maryland School of 
      Dentistry, Baltimore, MD, United States.
FAU - Pak, Joshua
AU  - Pak J
AD  - Department of Neural and Pain Sciences, University of Maryland School of 
      Dentistry, Baltimore, MD, United States.
FAU - Da Silva, Joyce Teixeira
AU  - Da Silva JT
AD  - Department of Neural and Pain Sciences, University of Maryland School of 
      Dentistry, Baltimore, MD, United States.
FAU - Ro, Jin Y
AU  - Ro JY
AD  - Department of Neural and Pain Sciences, University of Maryland School of 
      Dentistry, Baltimore, MD, United States.
LA  - eng
PT  - Journal Article
DEP - 20230530
PL  - Switzerland
TA  - Front Pain Res (Lausanne)
JT  - Frontiers in pain research (Lausanne, Switzerland)
JID - 9918227269806676
PMC - PMC10261988
OTO - NOTNLM
OT  - antioxidant
OT  - hyperalgesia
OT  - inflammation
OT  - muscle pain
OT  - oxidative stress
OT  - sensory ganglia
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2023/06/16 06:42
MHDA- 2023/06/16 06:43
PMCR- 2023/05/30
CRDT- 2023/06/16 04:27
PHST- 2023/04/11 00:00 [received]
PHST- 2023/05/16 00:00 [accepted]
PHST- 2023/06/16 06:43 [medline]
PHST- 2023/06/16 06:42 [pubmed]
PHST- 2023/06/16 04:27 [entrez]
PHST- 2023/05/30 00:00 [pmc-release]
AID - 10.3389/fpain.2023.1204057 [doi]
PST - epublish
SO  - Front Pain Res (Lausanne). 2023 May 30;4:1204057. doi: 
      10.3389/fpain.2023.1204057. eCollection 2023.