PMID- 23246844
OWN - NLM
STAT- MEDLINE
DCOM- 20131017
LR  - 20130415
IS  - 1873-7544 (Electronic)
IS  - 0306-4522 (Linking)
VI  - 239
DP  - 2013 Jun 3
TI  - Mechanisms underlying the interactions between rapid estrogenic and BDNF control 
      of synaptic connectivity.
PG  - 17-33
LID - S0306-4522(12)01184-0 [pii]
LID - 10.1016/j.neuroscience.2012.12.004 [doi]
AB  - The effects of the steroid hormone 17beta-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 
      17beta-estradiol on dendritic spines, via its ability to regulate the expression of 
      neurotrophins. Here we focus on the acute, or rapid effects, of 17beta-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 17beta-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 17beta-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 
      17beta-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.
CI  - Copyright (c) 2012 IBRO. All rights reserved.
FAU - Srivastava, D P
AU  - Srivastava DP
AD  - 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
FAU - Woolfrey, K M
AU  - Woolfrey KM
FAU - Evans, P D
AU  - Evans PD
LA  - eng
GR  - Biotechnology and Biological Sciences Research Council/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20121213
PL  - United States
TA  - Neuroscience
JT  - Neuroscience
JID - 7605074
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Estrogens)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - Dendritic Spines/metabolism
MH  - Estrogens/*metabolism
MH  - Humans
MH  - Neuronal Plasticity/physiology
MH  - Signal Transduction/*physiology
MH  - Synapses/*physiology
MH  - Synaptic Transmission/physiology
EDAT- 2012/12/19 06:00
MHDA- 2013/10/18 06:00
CRDT- 2012/12/19 06:00
PHST- 2012/11/19 00:00 [received]
PHST- 2012/12/03 00:00 [revised]
PHST- 2012/12/04 00:00 [accepted]
PHST- 2012/12/19 06:00 [entrez]
PHST- 2012/12/19 06:00 [pubmed]
PHST- 2013/10/18 06:00 [medline]
AID - S0306-4522(12)01184-0 [pii]
AID - 10.1016/j.neuroscience.2012.12.004 [doi]
PST - ppublish
SO  - Neuroscience. 2013 Jun 3;239:17-33. doi: 10.1016/j.neuroscience.2012.12.004. Epub 
      2012 Dec 13.