17 beta-estradiol (E2) promotes growth and stability of new dendritic spines via estrogen receptor beta pathway in intact mouse cortex

摘要

The steroid hormone 17 beta-estradiol (E2) remodels neural circuits at the synaptic level in the mammalian hippocampus and cortex. However, the underlying mechanism of synapse dynamics remains unclear. To elucidate the mechanism, we traced individual dendritic spines on layer V pyramidal neurons of the primary sensory cortex in adult female mice under E2 intervention using two-photon in vivo imaging microscopy. We confirmed the increase of the spine density upon E2 treatment in the intact mouse cortex. Furthermore, we found that this increase is due to the promotion of spine formation and the stability of newly formed spines. E2 treatment doesn't alter the elimination rate of pre-existing spines. Our results also indicate that the activation of the estrogen receptor beta (ER beta) mimics the effects of E2 administration on spine dynamics. Taken together, our findings suggest that estrogen promotes growth and stability of new dendritic spines via the ER beta pathway in the intact cortex of female mice.