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Year : 2019  |  Volume : 62  |  Issue : 5  |  Page : 175-181

Action of citral on the substantia gelatinosa neurons of the trigeminal subnucleus caudalis in juvenile mice

1 Department of Oral Physiology, School of Dentistry and Institute of Oral Bioscience, Jeonbuk National University, Jeonju, Republic of Korea; Faculty of Odonto – Stomatology, Hue University of Medicine and Pharmacy, Hue University, Hue, Vietnam
2 Department of Oral Physiology, School of Dentistry and Institute of Oral Bioscience, Jeonbuk National University, Jeonju, Republic of Korea
3 Department of Obstetrics and Gynecology, Jeonbuk National University Hospital-Jeonbuk, National University Medical School, Jeonju, Republic of Korea

Correspondence Address:
Prof. Dong Hyu Cho
20 Geonji-ro, Deokjin-gu, Jeonju-si, Jeollabuk-do, 54907
Republic of Korea
Prof. Seong Kyu Han
567 Baekje-daero, Deokjin-gu, Jeonju-si, Jeollabuk-do, 54896
Republic of Korea
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/CJP.CJP_32_19

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The substantia gelatinosa (SG) of the trigeminal subnucleus caudalis (Vc) is admitted as a pivotal site of integrating and regulating orofacial nociceptive inputs. Although citral (3,7-dimethyl-2,6-octadienal) is involved in antinociception, the action mechanism of citral on the SG neurons of the Vc has not been fully clarified yet. In this study, we examined the direct membrane effects of citral and how citral mediates responses on the SG neurons of the Vc in juvenile mice using a whole-cell patch-clamp technique. Under high chloride pipette solution, citral showed repeatable inward currents that persisted in the presence of tetrodotoxin, a voltage-gated Na+ channel blocker, and 6-cyano-7-nitro-quinoxaline-2,3-dione, a non-N-methyl-D-aspartate (NMDA) glutamate receptor antagonist, D-2-amino-5-phosphonopentanoic acid, an NMDA receptor antagonist. However, the citral-induced inward currents were partially blocked by picrotoxin, a gamma-aminobutyric acid (GABAA)-receptor antagonist, or by strychnine, a glycine receptor antagonist. Further, the citral-induced responses were almost blocked by picrotoxin with strychnine. We also found that citral exhibited additive effect with GABA-induced inward currents and glycine-induced inward currents were potentiated by citral. In addition, citral suppressed the firing activities by positive current injection on the SG neurons of the Vc. Taken together, these results demonstrate that citral has glycine- and/or GABA-mimetic actions and suggest that citral might be a potential target for orofacial pain modulation by the activation of inhibitory neurotransmission in the SG area of the Vc.

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