• D P Srivastava, K M Woolfrey, and P D Evans.
• Department of Neuroscience & Centre for the Cellular Basis of Behaviour, The James Black Centre, Institute of Psychiatry, King's College London, London SE5 9NU, UK. deepak.srivastava@kcl.ac.uk
• Neuroscience. 2013 Jun 3;239:17-33.

AbstractThe effects of the steroid hormone 17β-estradiol and the neurotrophin brain-derived neurotrophic factor (BDNF) on neuronal physiology have been well investigated. Numerous studies have demonstrated that each signal can exert powerful influences on the structure and function of synapses, and specifically on dendritic spines, both within short and long time frames. Moreover, it has been suggested that BDNF is required for the long-term, or genomic, actions of 17β-estradiol on dendritic spines, via its ability to regulate the expression of neurotrophins. Here we focus on the acute, or rapid effects, of 17β-estradiol and BDNF, and their ability to activate specific signalling cascades, resulting in alterations in dendritic spine morphology. We first review recent literature describing the mechanisms by which 17β-estradiol activates these pathways, and the resulting alterations in dendritic spine number. We then describe the molecular mechanisms underlying acute modulation of dendritic spine morphology by BDNF. Finally, we consider how this new evidence may suggest that the temporal interactions of 17β-estradiol and BDNF can occur more rapidly than previously reported. Building on these new data, we propose a novel model for the interactions of this steroid and neurotrophin, whereby rapid, non-genomic 17β-estradiol and acute BDNF signal in a co-operative manner, resulting in dendritic spine formation and subsequent stabilization in support of synapse and circuit plasticity. This extended hypothesis suggests an additional mechanism by which these two signals may modulate dendritic spines in a time-specific manner.Copyright © 2012 IBRO. All rights reserved.

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