Membrane-initiated estrogen signaling in hypothalamic neurons

Research output: Contribution to journalArticle

88 Citations (Scopus)

Abstract

It is well known that many of the actions of 17β-estradiol (E2) in the central nervous system are mediated via intracellular receptor/transcription factors that interact with steroid response elements on target genes. However, there is compelling evidence for membrane steroid receptors for estrogen in hypothalamic and other brain neurons. But it is not well understood how estrogen signals via membrane receptors, and how these signals impact not only membrane excitability but also gene transcription in neurons. Indeed, it has been known for sometime that E2 can rapidly alter neuronal activity within seconds, indicating that some cellular effects can occur via membrane delimited events. In addition, E2 can affect second messenger systems including calcium mobilization and a plethora of kinases to alter cell signaling. Therefore, this review will consider our current knowledge of rapid membrane-initiated and intracellular signaling by E2 in the hypothalamus, the nature of receptors involved and how they contribute to homeostatic functions.

Original languageEnglish (US)
Pages (from-to)14-23
Number of pages10
JournalMolecular and Cellular Endocrinology
Volume290
Issue number1-2
DOIs
StatePublished - Aug 13 2008

Fingerprint

Neurons
Estrogens
Membranes
Intracellular Membranes
Genes
Steroid Receptors
Cell signaling
Response Elements
Second Messenger Systems
Hypothalamus
Neurology
Estradiol
Transcription
Transcription Factors
Phosphotransferases
Central Nervous System
Steroids
Calcium
Brain

Keywords

  • ERα
  • ERβ
  • G protein-coupled receptor (GPCR)
  • Membrane estrogen receptor that is a GPCR (mER)

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Membrane-initiated estrogen signaling in hypothalamic neurons. / Kelly, Martin; Ronnekleiv, Oline.

In: Molecular and Cellular Endocrinology, Vol. 290, No. 1-2, 13.08.2008, p. 14-23.

Research output: Contribution to journalArticle

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