In Vivo Dissection of Two Intracellular Pathways Involved in the Spinal Oxytocin-Induced Antinociception in the Rat


Por: Espinosa De los Monteros-Zuniga, Antonio, Martinez-Lorenzana, Guadalupe, Condes-Lara, Miguel, Gonzalez-Hernandez, Abimael

Publicada: 18 ago 2021
Resumen:
Behavioral and electrophysiological data show that at the spinal level, oxytocin inhibits pain transmission by activation of oxytocin receptors (OTRs). Canonically, OTRs are coupled to Gq proteins, which induce a rise of intracellular Ca2+ by activating the phospholipase C (PLC). However, in vitro data showed that OTRs cause a plethora of intracellular events, some related to the activation of Gi proteins. Using a behavioral approach, we analyzed the main in vivo intracellular pathway elicited by spinal oxytocin during a peripheral inflammatory/persistent nociceptive stimulus. Intrathecal oxytocin reduces early (number of flinches) and late (mechanical allodynia) formalin-induced nociception, an effect abolished by the OTR antagonist (L-368,899). Furthermore, the antinociception observed during the early phase (acute inflammatory) was also reverted by U-73122 (PLC inhibitor) but not by pertussis toxin (G alpha(i/o) protein inhibitor) or gallein (G(beta gamma) subunit inhibitor). In contrast, the late oxytocin-induced behavioral analgesia was blocked by pertussis and gallein but not by U-73122. Since oxytocin's effects during the early phase were also antagonized by Nco-nitro-L-arginine methyl ester, ODQ, or glibenclamide (inhibitors of nitric oxide synthase [NOS], soluble guanylyl cyclase [GC], and K-ATP(+) channels, respectively), the role of two differential pathways elicited by oxytocin is supported. Hence, we showed in in vivo experiments that oxytocin recruits two differential spinal intracellular pathways mediated by Gq (PLC/NOS/GC/K-ATP(+)) or Gi proteins during a peripheral nociceptive stimulus.

Filiaciones:
Espinosa De los Monteros-Zuniga, Antonio:
 Gonzalez-Hernandez, A (Corresponding Author), Univ Nacl Autonoma Mexico, Inst Neurobiol, Dept Neurobiol Desarrollo & Neurofisiol, Queretaro 76230, Qro, Mexico. Espinosa De los Monteros-Zuniga, Antonio

Martinez-Lorenzana, Guadalupe:
 Gonzalez-Hernandez, A (Corresponding Author), Univ Nacl Autonoma Mexico, Inst Neurobiol, Dept Neurobiol Desarrollo & Neurofisiol, Queretaro 76230, Qro, Mexico. Espinosa De los Monteros-Zuniga, Antonio

Condes-Lara, Miguel:
 Gonzalez-Hernandez, A (Corresponding Author), Univ Nacl Autonoma Mexico, Inst Neurobiol, Dept Neurobiol Desarrollo & Neurofisiol, Queretaro 76230, Qro, Mexico. Espinosa De los Monteros-Zuniga, Antonio

Gonzalez-Hernandez, Abimael:
 Gonzalez-Hernandez, A (Corresponding Author), Univ Nacl Autonoma Mexico, Inst Neurobiol, Dept Neurobiol Desarrollo & Neurofisiol, Queretaro 76230, Qro, Mexico. Espinosa De los Monteros-Zuniga, Antonio
ISSN: 19487193





ACS CHEMICAL NEUROSCIENCE
Editorial
AMER CHEMICAL SOC, 1155 16TH ST, NW, WASHINGTON, DC 20036 USA, Estados Unidos America
Tipo de documento: Article
Volumen: 12 Número: 16
Páginas: 3140-3147
WOS Id: 000687176700016
ID de PubMed: 34342984

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