¹Department of Biomedical Sciences, Atlantic Veterinary College, University of Prince Edward Island, Charlottetown, PE, Canada

Correspondence: Dr M Fatehi, Department of Physiology and Biophysics, Faculty of Medicine, Dalhousie University, Halifax, NS, Canada B3H 1X5. Tel: +1 902 494 2265; Fax: +1 902 494 1685; E-mail: mohfatehi@yahoo.com

Received 6 April 2007; Revised 4 June 2007; Accepted 9 July 2007; Published online 8 August 2007.

Abstract

17-Estradiol receptors have been found in several brain nuclei including the suprachiasmatic nucleus (SCN) of mammalian species. The SCN is believed to act as brain clock regulating circadian and circannual biological rhythms, such as body temperature, sleep, and mood. Here, we examined whether 17-estradiol (E₂) could affect cell excitability and synaptic transmission in the SCN. Bath application of E₂ (0.03–3 M) increased the spontaneous firing frequency and depolarized cell membrane of the SCN neurons significantly. Furthermore, E₂ (0.03–3 M) increased (by about 25–150% of control) frequency of the miniature excitatory postsynaptic currents. Amplitude of the evoked excitatory postsynaptic currents was enhanced (by about 32% of control) after exposure to 1 M E₂. The paired-pulse ratio was reduced by E₂. These effects were prevented by the estrogen receptor antagonist, ICI 182780. Exposure to the biologically inactive 17-estradiol did not cause any significant changes in the parameters mentioned above. These findings are in favor of an implication of estrogen in modulation of neuronal activity in SCN and possibly regulating circadian rhythms.