Abstract
Recent studies have provided several lines of evidence that peripheral administration of oxytocin induces analgesia in human and rodents. However, the exact underlying mechanism of analgesia still remains elusive. In the present study, we aimed to identify which receptor could mediate the analgesic effect of intraperitoneal injection of oxytocin and its cellular mechanisms in thermal pain behavior. We found that oxytocin-induced analgesia could be reversed by d(CH2)5[Tyr(Me)2, Dab5] AVP, a vasopressin-1a (V1a) receptor antagonist, but not by desGly-NH2-d(CH2)5[DTyr2, Thr4]OVT, an oxytocin receptor antagonist. Single cell RT-PCR analysis revealed that V1a receptor, compared to oxytocin, vasopressin-1b and vasopressin-2 receptors, was more profoundly expressed in dorsal root ganglion (DRG) neurons and the expression of V1a receptor was predominant in transient receptor potential vanilloid 1 (TRPV1)-expressing DRG neurons. Fura-2 based calcium imaging experiments showed that capsaicin-induced calcium transient was significantly inhibited by oxytocin and that such inhibition was reversed by V1a receptor antagonist. Additionally, whole cell patch clamp recording demonstrated that oxytocin significantly increased potassium conductance via V1a receptor in DRG neurons. Taken together, our findings suggest that analgesic effects produced by peripheral administration of oxytocin were attributable to the activation of V1a receptor, resulting in reduction of TRPV1 activity and enhancement of potassium conductance in DRG neurons.
| Original language | English |
|---|---|
| Pages (from-to) | 173-182 |
| Number of pages | 10 |
| Journal | Korean Journal of Physiology and Pharmacology |
| Volume | 22 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - 2018 Mar 1 |
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Keywords
- Dorsal root ganglion
- Electrophysiology
- Oxytocin
- Pain
- Vasopressin receptor
ASJC Scopus subject areas
- Physiology
- Pharmacology
Cite this
Oxytocin produces thermal analgesia via vasopressin-1a receptor by modulating TRPV1 and potassium conductance in the dorsal root ganglion neurons. / Han, Rafael Taeho; Kim, Han Byul; Kim, Young Beom; Choi, Kyungmin; Park, Gi Yeon; Lee, Pa Reum; Lee, Jaehee; Kim, Hye Young; Park, Chul Kyu; Kang, Youngnam; Oh, Seog Bae; Na, Heung Sik.
In: Korean Journal of Physiology and Pharmacology, Vol. 22, No. 2, 01.03.2018, p. 173-182.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Oxytocin produces thermal analgesia via vasopressin-1a receptor by modulating TRPV1 and potassium conductance in the dorsal root ganglion neurons
AU - Han, Rafael Taeho
AU - Kim, Han Byul
AU - Kim, Young Beom
AU - Choi, Kyungmin
AU - Park, Gi Yeon
AU - Lee, Pa Reum
AU - Lee, Jaehee
AU - Kim, Hye Young
AU - Park, Chul Kyu
AU - Kang, Youngnam
AU - Oh, Seog Bae
AU - Na, Heung Sik
PY - 2018/3/1
Y1 - 2018/3/1
N2 - Recent studies have provided several lines of evidence that peripheral administration of oxytocin induces analgesia in human and rodents. However, the exact underlying mechanism of analgesia still remains elusive. In the present study, we aimed to identify which receptor could mediate the analgesic effect of intraperitoneal injection of oxytocin and its cellular mechanisms in thermal pain behavior. We found that oxytocin-induced analgesia could be reversed by d(CH2)5[Tyr(Me)2, Dab5] AVP, a vasopressin-1a (V1a) receptor antagonist, but not by desGly-NH2-d(CH2)5[DTyr2, Thr4]OVT, an oxytocin receptor antagonist. Single cell RT-PCR analysis revealed that V1a receptor, compared to oxytocin, vasopressin-1b and vasopressin-2 receptors, was more profoundly expressed in dorsal root ganglion (DRG) neurons and the expression of V1a receptor was predominant in transient receptor potential vanilloid 1 (TRPV1)-expressing DRG neurons. Fura-2 based calcium imaging experiments showed that capsaicin-induced calcium transient was significantly inhibited by oxytocin and that such inhibition was reversed by V1a receptor antagonist. Additionally, whole cell patch clamp recording demonstrated that oxytocin significantly increased potassium conductance via V1a receptor in DRG neurons. Taken together, our findings suggest that analgesic effects produced by peripheral administration of oxytocin were attributable to the activation of V1a receptor, resulting in reduction of TRPV1 activity and enhancement of potassium conductance in DRG neurons.
AB - Recent studies have provided several lines of evidence that peripheral administration of oxytocin induces analgesia in human and rodents. However, the exact underlying mechanism of analgesia still remains elusive. In the present study, we aimed to identify which receptor could mediate the analgesic effect of intraperitoneal injection of oxytocin and its cellular mechanisms in thermal pain behavior. We found that oxytocin-induced analgesia could be reversed by d(CH2)5[Tyr(Me)2, Dab5] AVP, a vasopressin-1a (V1a) receptor antagonist, but not by desGly-NH2-d(CH2)5[DTyr2, Thr4]OVT, an oxytocin receptor antagonist. Single cell RT-PCR analysis revealed that V1a receptor, compared to oxytocin, vasopressin-1b and vasopressin-2 receptors, was more profoundly expressed in dorsal root ganglion (DRG) neurons and the expression of V1a receptor was predominant in transient receptor potential vanilloid 1 (TRPV1)-expressing DRG neurons. Fura-2 based calcium imaging experiments showed that capsaicin-induced calcium transient was significantly inhibited by oxytocin and that such inhibition was reversed by V1a receptor antagonist. Additionally, whole cell patch clamp recording demonstrated that oxytocin significantly increased potassium conductance via V1a receptor in DRG neurons. Taken together, our findings suggest that analgesic effects produced by peripheral administration of oxytocin were attributable to the activation of V1a receptor, resulting in reduction of TRPV1 activity and enhancement of potassium conductance in DRG neurons.
KW - Dorsal root ganglion
KW - Electrophysiology
KW - Oxytocin
KW - Pain
KW - Vasopressin receptor
UR - http://www.scopus.com/inward/record.url?scp=85043362120&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85043362120&partnerID=8YFLogxK
U2 - 10.4196/kjpp.2018.22.2.173
DO - 10.4196/kjpp.2018.22.2.173
M3 - Article
AN - SCOPUS:85043362120
VL - 22
SP - 173
EP - 182
JO - Korean Journal of Physiology and Pharmacology
JF - Korean Journal of Physiology and Pharmacology
SN - 1226-4512
IS - 2
ER -