Tracking the estrogen receptor in neurons: Implications for estrogen-induced synapse formation Review uri icon

Overview

MeSH Major

  • Estrogens
  • Neurons
  • Receptors, Estrogen
  • Synapses

abstract

  • Estrogens (E) and progestins regulate synaptogenesis in the CA1 region of the dorsal hippocampus during the estrous cycle of the female rat, and the functional consequences include changes in neurotransmission and memory. Synapse formation has been demonstrated by using the Golgi technique, dye filling of cells, electron microscopy, and radioimmunocytochemistry. N-methyl-d-aspartate (NMDA) receptor activation is required, and inhibitory interneurons play a pivotal role as they express nuclear estrogen receptor alpha (ERalpha) and show E-induced decreases of GABAergic activity. Although global decreases in inhibitory tone may be important, a more local role for E in CA1 neurons seems likely. The rat hippocampus expresses both ERalpha and ERbeta mRNA. At the light microscopic level, autoradiography shows cell nuclear [3H]estrogen and [125I]estrogen uptake according to a distribution that primarily reflects the localization of ERalpha-immunoreactive interneurons in the hippocampus. However, recent ultrastructural studies have revealed extranuclear ERalpha immunoreactivity (IR) within select dendritic spines on hippocampal principal cells, axon terminals, and glial processes, localizations that would not be detectable by using standard light microscopic methods. Based on recent studies showing that both types of ER are expressed in a form that activates second messenger systems, these findings support a testable model in which local, non-genomic regulation by estrogen participates along with genomic actions of estrogens in the regulation of synapse formation.

publication date

  • June 19, 2001

Research

keywords

  • Review

Identity

Language

  • eng

PubMed Central ID

  • PMC34628

Digital Object Identifier (DOI)

  • 10.1073/pnas.121146898

PubMed ID

  • 11416193

Additional Document Info

start page

  • 7093

end page

  • 100

volume

  • 98

number

  • 13