Evidence map›Paper›PMID 20333733›Full record

ArticleHippocampus2011

Kalirin-7, an important component of excitatory synapses, is regulated by estradiol in hippocampal neurons.

Xin-Ming Ma, Jian-Ping Huang, Eun-Ji Kim, Qing Zhu, George A Kuchel, Richard E Mains, Betty A Eipper

Abstract read
In one paragraph

Article in Hippocampus, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.0field-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

31 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
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  8. Review
  9. Genetic Variant ofBioMed research international · 2017
    Article
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  13. Review
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  16. Reversing synapse loss in Alzheimer's disease: Rho-guanosine triphosphatases and insights from other brain disorders.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2015
    Review
  17. Article
  18. Article
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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

7 authors at 1 institution in 1 country.

Xin-Ming MaDepartment of Neuroscience, University of Connecticut Health Center, Farmington, 06030, USA. ma@nso.uchc.edu
Jian-Ping Huang
Eun-Ji Kim
Qing Zhu
George A Kuchel
Richard E Mains
Betty A Eipper
UConn Health · US

Funding

Dissecting the role of one neuronal RhoGEF amongst many: the Kalirin-7 null mouseR01DA023082 · NIDA · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI MAINS, RICHARD E · 2008 to 2012
$1.6M
GDP/GTP Exchange Factors: Nucleus Accumbens PlasticityR01DA015464 · NIDA · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI EIPPER, ELIZABETH ANNE · 2004 to 2008
$1.6M
NIDA NIH HHS DA-15464NIDA NIH HHS R01 DA015464NIDA NIH HHS R01 DA023082
6 · The paper itself

Abstract

Estradiol enhances the formation of dendritic spines and excitatory synapses in hippocampal neurons in vitro and in vivo, but the underlying mechanisms are not fully understood. Kalirin-7 (Kal7), the major isoform of Kalirin in the adult hippocampus, is a Rho GDP/GTP exchange factor localized to postsynaptic densities. In the hippocampus, both Kal7 and estrogen receptor α (ERα) are highly expressed in a subset of interneurons. Over-expression of Kal7 caused an increase in spine density and size in hippocampal neurons. To determine whether Kalirin might play a role in the effects of estradiol on spine formation, Kal7 expression was examined in the hippocampus of ovariectomized rats. Estradiol replacement increased Kal7 staining in both CA1 pyramidal neurons and interneurons in ovariectomized rats. Estradiol treatment of cultured hippocampal neurons increased Kal7 levels at the postsynaptic side of excitatory synapses and increased the number of excitatory synapses along the dendrites of pyramidal neurons. These increases were mediated via ERα because a selective ERα agonist, but not a selective ERβ agonist, caused a similar increase in both Kal7 levels and excitatory synapse number in cultured hippocampal neurons. When Kal7 expression was reduced using a Kal7-specific shRNA, the density of excitatory synapses was reduced and estradiol was no longer able to increase synapse formation. Expression of exogenous Kal7 in hippocampal interneurons resulted in decreased levels of GAD65 staining. Inhibition of GABAergic transmission with bicuculline produced a robust increase in Kal7 expression. These studies suggest Kal7 plays a key role in the mechanisms of estradiol-mediated synaptic plasticity.

Indexed as

EstradiolEstrogen Receptor alphaAnimalsCA1 Region, HippocampalCells, CulturedDendritic SpinesEstrogen Receptor betaExcitatory Postsynaptic PotentialsFemaleGABA-A Receptor AgonistsGABA-B Receptor AgonistsGlutamate DecarboxylaseGuanine Nucleotide Exchange FactorsImmunohistochemistryInterneuronsNeurogenesisEstradiolEstrogen Receptor alphaEstrogen Receptor betaGABA-A Receptor AgonistsGABA-B Receptor AgonistsGlutamate Decarboxylaseglutamate decarboxylase 2Guanine Nucleotide Exchange FactorsKalrn protein, ratRNA, Small Interfering

Identifiers

PMID20333733
PMCPMC2911517
OpenAlexW2082499181

What Socratic 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 Socratic graph.