Enhancement of rat hippocampal long-term potentiation by 17 beta-estradiol involves mitogen-activated protein kinase-dependent and -independent components

Neurosci Lett. 2002 Oct 25;332(1):65-9. doi: 10.1016/s0304-3940(02)00902-3.

Abstract

To investigate if estrogen modulates long-term potentiation (LTP) via mitogen-activated protein kinase (MAPK) activation, in vitro hippocampal slices were used to induce LTP through extracellular field recordings. Slices perfused with 17beta-estradiol exhibited a significant enhancement of LTP (224+/-19%) compared with LTP in control slices (157+/-9%). In the presence of PD098059, 17beta-estradiol still produced a significant magnitude of LTP (131+/-7%), revealing the existence of p-MAPK-independent LTP mediated by 17beta-estradiol. Immunocytochemistry showed that 17beta-estradiol promoted a transient increase in nuclear translocation of p-MAPK. 17beta-estradiol induced the extracellular proteolysis of neural cell adhesion molecule in a p-MAPK-independent manner, indicating that 17beta-estradiol may act on synaptic remodeling. These results indicate that 17beta-estradiol might affect hippocampal synaptic plasticity in a way involving two separate pathways, which are MAPK-dependent and MAPK-independent.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Estradiol / pharmacology*
  • Hippocampus / drug effects*
  • Hippocampus / enzymology*
  • In Vitro Techniques
  • Long-Term Potentiation / drug effects*
  • Long-Term Potentiation / physiology
  • Male
  • Mitogen-Activated Protein Kinases / physiology*
  • Rats
  • Rats, Sprague-Dawley

Substances

  • Estradiol
  • Mitogen-Activated Protein Kinases