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conferenceseries.com
Volume 6, Issue 5 (Suppl) J Pain Relief, an open access journal
ISSN: 2167-0846 Pain Management 2017
October 05-06, 2017
5th International Conference and Exhibition on
October 05-06, 2017 London, UK
Pain Research And Management
COX2/PGE2/EP4 signaling is involved in repeated restraint stress predisposed transition from acute
to chronic pain
Weiya Ma 1,2
1Douglas Mental Health University Institute, Canada
2McGill University, Canada
Chronic pain is a serious health issue that afflicts >20% of the population and causes the worst quality of life. Its treatments
are challenging due to unclear mechanisms. Emerging evidence suggest that sensitization of nociceptive neurons along
peripheral (dorsal root ganglion, DRG) and central (dorsal horn and brain) pain pathways contributes to chronic pain.
Prevalence of prior stress experience is linked to high incidence of chronic pain. Stress, particularly repeated stress, induces
maladaptive neuroplasticity along peripheral and central pain pathways. These plastic events facilitate persistent sensitization
of nociceptive neurons and transition from acute to chronic pain. Prostaglandin E2 (PGE2), a pain mediator enriched in
injured tissues, is involved in chronic pain. Its EP4 receptor, a major player in pathological pain conditions, is considered as
a potential therapeutic target of chronic pain. In this study, we examined whether COC2/PGE2/EP4 signaling is involved in
stress-prolonged sensitization pain, a model for transition from acute to chronic pain. We found that pre-exposure to single
restraint stress abolished sensitization pain evoked by subsequent PGE2 challenge. However, pre-exposure to 3d consecutive
restraint stress not only prolonged sensitization pain evoked by PGE2, but also increased stress hormone corticosterone (CORT)
in serum, COX2 levels in paw skin, EP4 and TRPV1 levels in DRG and paw skin. Pre-exposure to CORT for 3d also prolonged
pain evoked by PGE2 while co-injection of glucocorticoid receptor (GR) antagonist RU486 with 3d restraint stress prevented
prolongation of sensitization pain. Co-injection of a selective COX2 inhibitor NS-398 or a selective EP4 receptor antagonist
L161,982 attenuated 3d restraint stress prolonged sensitization pain. In DRG cultures, in a concentration-dependent manner,
CORT induced an increase in EP4 and TRPV1 protein levels via GR activation. These data suggest that stress-up-regulated
COX2/PGE2/EP4 signaling and TRPV1 channel in peripheral pain pathway contribute to stress-predisposed transition from
acute to chronic pain.
Biography
Weiya Ma earned her PhD from Dept. of Pharmacology and Therapeutics at McGill University, Canada. She is now a Faculty Member at Douglas Institute and Dept.
of Psychiatry, McGill University, Montreal, Canada. Thus far she has published more than 70 research articles and numerous book chapters. Her studies unraveled
the role of neuropeptides in chronic pain conditions and morphine tolerance. Her pioneer work exploring the role of PGE2 in neuropathic pain and prolonged
sensitization pain has let her become a Leader in this field.
Weiya Ma, J Pain Relief 2017, 6:5(Suppl)
DOI: 10.4172/2167-0846-C1-014