These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Arginine vasopressin antagonizes the effects of prostaglandin E2 on the spontaneous activity of warm-sensitive and temperature-insensitive neurons in the medial preoptic area in rats.
    Author: Xu JH, Hou XY, Tang Y, Luo R, Zhang J, Liu C, Yang YL.
    Journal: Neurosci Lett; 2018 Jan 01; 662():59-64. PubMed ID: 28988972.
    Abstract:
    Arginine vasopressin (AVP) plays an important role in thermoregulation and antipyresis. We have demonstrated that AVP could change the spontaneous activity of thermosensitive and temperature insensitive neurons in the preoptic area. However, whether AVP influences the effects of prostaglandin E2 (PGE2) on the spontaneous activity of neurons in the medial preoptic area (MPO) remains unclear. Our experiment showed that PGE2 decreased the spontaneous activity of warm-sensitive neurons, and increased that of low-slope temperature-insensitive neurons in the MPO. AVP attenuated the inhibitory effect of PGE2 on warm-sensitive neurons, and reversed the excitatory effect of PGE2 on low-slope temperature-insensitive neurons, demonstrating that AVP antagonized the effects of PGE2 on the spontaneous activity of these neurons. The effect of AVP was suppressed by an AVP V1a receptor antagonist, suggesting that V1a receptor mediated the action of AVP. We also demonstrated that AVP attenuated the PGE2-induced decrease in the prepotential's rate of rise in warm-sensitive neurons and the PGE2-induced increase in that in low-slope temperature-insensitive neurons through the V1a receptor. Together, these data indicated that AVP antagonized the PGE2-induced change in the spontaneous activity of warm-sensitive and low-slope temperature-insensitive neurons in the MPO partly by reducing the PGE2-induced change in the prepotential of these neurons in a V1a receptor-dependent manner.
    [Abstract] [Full Text] [Related] [New Search]