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The Role of Prostaglandin E1 as a Pain Mediator through Facilitation of Hyperpolarization-Activated Cyclic Nucleotide-Gated Channel 2 via the EP2 Receptor in Trigeminal Ganglion Neurons of Mice

1
Department of Biological Sciences, Columbia University, New York, NY 10027, USA
2
Department of Physiology, College of Medicine, Hanyang University, Seoul 04763, Korea
3
Department of Anesthesiology and Pain Medicine, Seoul National University College of Medicine, Seoul 03080, Korea
*
Authors to whom correspondence should be addressed.
These authors have contributed equally to this work.
Academic Editor: Jean-Marc A. Lobaccaro
Int. J. Mol. Sci. 2021, 22(24), 13534; https://doi.org/10.3390/ijms222413534
Received: 14 November 2021 / Revised: 6 December 2021 / Accepted: 13 December 2021 / Published: 16 December 2021
(This article belongs to the Section Biochemistry)
Cyclooxygenase metabolizes dihomo-γ-linolenic acid and arachidonic acid to form prostaglandin (PG) E, including PGE1 and PGE2, respectively. Although PGE2 is well known to play an important role in the development and maintenance of hyperalgesia and allodynia, the role of PGE1 in pain is unknown. We confirm whether PGE1 induced pain using orofacial pain behavioral test in mice and determine the target molecule of PGE1 in TG neurons with whole-cell patch-clamp and immunohistochemistry. Intradermal injection of PGE1 to the whisker pads of mice induced a reduced threshold, enhancing the excitability of HCN channel-expressing trigeminal ganglion (TG) neurons. The HCN channel-generated inward current (Ih) was increased by 135.3 ± 4.8% at 100 nM of PGE1 in small- or medium-sized TG, and the action of PGE1 on Ih showed a concentration-dependent effect, with a median effective dose (ED50) of 29.3 nM. Adenylyl cyclase inhibitor (MDL12330A), 8-bromo-cAMP, and the EP2 receptor antagonist AH6809 inhibited PGE1-induced Ih. Additionally, PGE1-induced mechanical allodynia was blocked by CsCl and AH6809. PGE1 plays a role in mechanical allodynia through HCN2 channel facilitation via the EP2 receptor in nociceptive neurons, suggesting a potential therapeutic target in that PGE1 could be involved in pain as endogenous substances under inflammatory conditions. View Full-Text
Keywords: EP2; HCN2 channel; pain; PGE1; trigeminal ganglion neuron EP2; HCN2 channel; pain; PGE1; trigeminal ganglion neuron
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MDPI and ACS Style

Kwon, J.; Choi, Y.I.; Jo, H.J.; Lee, S.H.; Lee, H.K.; Kim, H.; Moon, J.Y.; Jung, S.J. The Role of Prostaglandin E1 as a Pain Mediator through Facilitation of Hyperpolarization-Activated Cyclic Nucleotide-Gated Channel 2 via the EP2 Receptor in Trigeminal Ganglion Neurons of Mice. Int. J. Mol. Sci. 2021, 22, 13534. https://doi.org/10.3390/ijms222413534

AMA Style

Kwon J, Choi YI, Jo HJ, Lee SH, Lee HK, Kim H, Moon JY, Jung SJ. The Role of Prostaglandin E1 as a Pain Mediator through Facilitation of Hyperpolarization-Activated Cyclic Nucleotide-Gated Channel 2 via the EP2 Receptor in Trigeminal Ganglion Neurons of Mice. International Journal of Molecular Sciences. 2021; 22(24):13534. https://doi.org/10.3390/ijms222413534

Chicago/Turabian Style

Kwon, Jean, Young I. Choi, Hang J. Jo, Sang H. Lee, Han K. Lee, Heesoo Kim, Jee Y. Moon, and Sung J. Jung. 2021. "The Role of Prostaglandin E1 as a Pain Mediator through Facilitation of Hyperpolarization-Activated Cyclic Nucleotide-Gated Channel 2 via the EP2 Receptor in Trigeminal Ganglion Neurons of Mice" International Journal of Molecular Sciences 22, no. 24: 13534. https://doi.org/10.3390/ijms222413534

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