Increased anxiety and synaptic plasticity in estrogen receptor β-deficient mice

  1. Wojciech Krȩżel*,
  2. Sonia Dupont,
  3. Andrée Krust,
  4. Pierre Chambon, and
  5. Paul F. Chapman*,
  1. *Cardiff School of Biosciences, Cardiff University, Museum Avenue, P.O. Box 911, Cardiff, CF10 3US, United Kingdom; and Institut de Génétique et de Biologie Moléculaire et Cellulaire, Centre National de la Recherche Scientifique/Institut National de la Santé et de la Recherche Médicale/Université Louis Pasteur, Collège de France, BP 163, 67404 Illkirch Cedex, France
  1. Contributed by Pierre Chambon

Abstract

Estrogens are powerful modulators of neuronal physiology and in humans may affect a broad range of functions, including reproductive, emotional, and cognitive behaviors. We studied the contribution of estrogen receptors (ERs) in modulation of emotional processes and analyzed the effects of deleting ERα or ERβ in mice. Behavior consistent with increased anxiety was observed principally in ERβ mutant females and was associated with a reduced threshold for the induction of synaptic plasticity in the basolateral amygdala. Local increase of 5-hydroxytryptamine 1a receptor expression in medial amygdala may contribute to these changes. Our data show that, particularly in females, there is an important role for ERβ-mediated estrogen signaling in the processing of emotional behavior.

Footnotes

  • To whom reprint requests should be addressed. E-mail: chapmanPF{at}cf.ac.uk.

  • § Koss, W. A., Sajdyk, T.J., Morin, S. M., Shekhar, A. & Gehlert, D.R. (2000) Meeting of the Society for Neuroscience, New Orleans, Nov. 2000, abstr. 659.3.

  • Rudick, C. N. & Woolley, C. S. (2000) Meeting of the Society for Neuroscience, New Orleans, Nov. 2000, abstr. 431.12.

  • Abbreviations:
    ER,
    estrogen receptor;
    WT,
    wild type;
    OF,
    open field;
    BLA,
    basolateral amygdala;
    LTP,
    long-term potentiation;
    GAD,
    glutamic acid decarboxylase;
    DAPI,
    4′,6-diamidino-2-phenylindole;
    Me,
    medial amygdala;
    VPL,
    ventral posterolateral thalamus;
    5-HT,
    5-hydroxytryptamine;
    GABA,
    γ-aminobutyric acid
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