DP Srivastava, KM Woolfrey, PD Evans
The effects of the steroid hormone 17脦虏-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 17脦虏-estradiol on dendritic spines, via its ability to regulate the expression of neurotrophins. Here we focus on the acute, or rapid effects, of 17脦虏-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 17脦虏-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 17脦虏-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 17脦虏-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.
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Neuroscience, PMID: 23246844
2013