Control of CNS neuronal excitability by estrogens via membrane-initiated signaling

Research output: Contribution to journalArticle

58 Citations (Scopus)

Abstract

It is well known that many of the actions of 17β-estradiol (E2) in the central nervous system (CNS) are mediated via intracellular receptor/transcription factors that interact with steroid response elements on target genes. However, there is compelling evidence for membrane-associated steroid receptors for E2 in hypothalamic and other brain neurons. Indeed, we are just beginning to understand how E2 signals via membrane receptors, and how these signals impact not only membrane excitability but also gene transcription in neurons. We know 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. This review will concentrate on rapid membrane-initiated and intracellular signaling by E2 in the hypothalamus and hippocampus, the nature of receptors involved and how they contribute to CNS functions.

Original languageEnglish (US)
Pages (from-to)17-25
Number of pages9
JournalMolecular and Cellular Endocrinology
Volume308
Issue number1-2
DOIs
StatePublished - Sep 24 2009

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

Keywords

  • ERα
  • ERβ
  • GPR30
  • mER (a plasma membrane E2 receptor that is G-protein-coupled)

ASJC Scopus subject areas

  • Endocrinology
  • Molecular Biology
  • Biochemistry

Cite this

Control of CNS neuronal excitability by estrogens via membrane-initiated signaling. / Kelly, Martin; Ronnekleiv, Oline.

In: Molecular and Cellular Endocrinology, Vol. 308, No. 1-2, 24.09.2009, p. 17-25.

Research output: Contribution to journalArticle

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