Britton Chance Center for Biomedical Photonics, Wuhan National Laboratory for Optoelectronics-Huazhong University of Science and Technology, Wuhan, Hubei 430074, China; MOE Key Laboratory for Biomedical Photonics, Collaborative Innovation Center for Biomedical Engineering, School of Engineering Sciences, Huazhong University of Science and Technology, Wuhan, Hubei 430074, China.
Chengdu Military General Hospital, Chengdu, China.
Brain Res Bull. 2018 Mar;137:241-248. doi: 10.1016/j.brainresbull.2017.12.011. Epub 2017 Dec 27.
The steroid hormone 17β-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 β (ERβ) 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 ERβ pathway in the intact cortex of female mice.
甾体激素 17β-雌二醇（E2）在哺乳动物海马体和皮质的突触水平重塑神经回路。然而，突触动态的潜在机制仍不清楚。为了阐明这一机制，我们使用双光子在体成像显微镜在雌性成年小鼠的初级感觉皮层的 V 层锥体神经元上追踪单个树突棘，在 E2 干预下。我们证实 E2 处理可增加完整小鼠皮质中的棘密度。此外，我们发现这种增加是由于促进了棘形成和新形成的棘的稳定性。E2 处理不会改变预先存在的棘的消除率。我们的结果还表明，雌激素受体 β（ERβ）的激活模拟了 E2 给药对棘动力学的影响。总之，我们的研究结果表明，雌激素通过雌性小鼠完整皮质中的 ERβ 途径促进新树突棘的生长和稳定性。
