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Cell signaling dependence of rapid glucocorticoid-induced endocannabinoid synthesis in hypothalamic neuroendocrine cells.

Authors
  • Harris, Christina1
  • Weiss, Grant L1
  • Di, Shi1
  • Tasker, Jeffrey G1, 2
  • 1 Department of Cell and Molecular Biology, Tulane University, New Orleans, LA, USA.
  • 2 Tulane Brain Institute, Tulane University, New Orleans, LA, USA.
Type
Published Article
Journal
Neurobiology of stress
Publication Date
Feb 01, 2019
Volume
10
Pages
100158–100158
Identifiers
DOI: 10.1016/j.ynstr.2019.100158
PMID: 31193551
Source
Medline
Language
English
License
Unknown

Abstract

Glucocorticoids induce a rapid synthesis of endocannabinoid in hypothalamic neuroendocrine cells by activation of a putative membrane receptor. Somato-dendritically released endocannabinoid acts as a retrograde messenger to suppress excitatory synaptic inputs to corticotropin-releasing hormone-, oxytocin-, and vasopressin-secreting cells. The non-genomic signaling mechanism responsible for rapid endocannabinoid synthesis by glucocorticoids has yet to be fully characterized. Here we manipulated cell signaling molecules pharmacologically using an intracellular approach to elucidate the signaling pathway activated by the membrane glucocorticoid receptor in hypothalamic neuroendocrine cells. We found that rapid glucocorticoid-induced endocannabinoid synthesis in magnocellular neuroendocrine cells requires the sequential activation of multiple kinases, phospholipase C, and intracellular calcium mobilization. While there remain gaps in our understanding, our findings reveal many of the critical players in the rapid glucocorticoid signaling that culminates in the retrograde endocannabinoid modulation of excitatory synaptic transmission.

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