Evidence map›Paper›PMID 24112361›Full record

ReviewJournal of neuroendocrinology2013

Rapid effects of oestrogen on synaptic plasticity: interactions with actin and its signalling proteins.

A H Babayan, E A Kramár

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of neuroendocrinology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.1field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 49 citations in OpenAlex.

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  19. Estradiol and hippocampal memory in female and male rodents.Current opinion in behavioral sciences · 2018
    Article
  20. Pregnancy: Effect on Multiple Sclerosis, Treatment Considerations, and Breastfeeding.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2017
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

A H BabayanDepartment of Anatomy and Neurobiology, University of California, Irvine, CA, USA.
E A Kramár
University of California, Irvine · US

Funding

The Spine Cytoskeleton and Memory DisordersP01NS045260 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI GALL, CHRISTINE M · 2003 to 2015
$14.4M
Fragile X and Synaptic PlasticityR01MH082042 · NIMH · UNIVERSITY OF CALIFORNIA-IRVINE · PI GALL, CHRISTINE M, LAUTERBORN, JULIE C · 2009 to 2012
$1.5M
NIMH NIH HHS MH082042NIMH NIH HHS R01 MH082042NINDS NIH HHS NS045260NINDS NIH HHS P01 NS045260
6 · The paper itself

Abstract

Oestrogen rapidly enhances fast excitatory postsynaptic potentials, facilitates long-term potentiation (LTP) and increases spine numbers. Each effect likely contributes to the influence of the steroid on cognition and memory. In the present review, we first describe a model for the substrates of LTP that includes an outline of the synaptic events occurring during induction, expression and consolidation. Briefly, critical signalling pathways involving the small GTPases RhoA and Rac/Cdc42 are activated by theta burst-induced calcium influx and initiate actin filament assembly via phosphorylation (inactivation) of cofilin. Reorganisation of the actin cytoskeleton changes spine and synapse morphology, resulting in increased concentrations of AMPA receptors at stimulated contacts. We then use the synaptic model to develop a specific hypothesis about how oestrogen affects both baseline transmission and plasticity. Brief infusions of 17β-oestradiol (E2 ) reversibly stimulate the RhoA, cofilin phosphorylation and actin polymerisation cascade of the LTP machinery; blocking this eliminates the effects of the steroid on transmission. We accordingly propose that E2 induces a weak form of LTP and thereby increases synaptic responses, a hypothesis that also accounts for how it markedly enhances theta burst induced potentiation. Although the effects of E2 on the cytoskeleton could be a result of the direct activation of small GTPases by oestrogen receptors on the synaptic membrane, the hormone also activates tropomyosin-related kinase B receptors for brain-derived neurotrophic factor, a neurotrophin that engages the RhoA-cofilin sequence and promotes LTP. The latter observations raise the possibility that E2 produces its effects on synaptic physiology via transactivation of neighbouring receptors that have prominent roles in the management of spine actin, synaptic physiology and plasticity.

Indexed as

ActinsAnimalsEstrogensLong-Term PotentiationNeuronal PlasticitySignal TransductionSynapsesActinsEstrogenscofilinlong-term potentiationoestradiolpTrkBRhoAspines

Identifiers

PMID24112361
PMCPMC3989941
OpenAlexW1974152416

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.