Evidence map›Paper›PMID 20817852›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

Axonal α7 nicotinic ACh receptors modulate presynaptic NMDA receptor expression and structural plasticity of glutamatergic presynaptic boutons.

Hong Lin, Stefano Vicini, Fu-Chun Hsu, Shachee Doshi, Hajime Takano, Douglas A Coulter, David R Lynch

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

30 citing papers in PubMed, 67 citations in OpenAlex.

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  6. Nicotinic acetylcholine receptor subunit αJournal of neurophysiology · 2019
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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 4 institutions in 1 country.

Hong LinDepartment of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.
Stefano Vicini
Fu-Chun Hsu
Shachee Doshi
Hajime Takano
Douglas A Coulter
David R Lynch
Children's Hospital of Philadelphia · USPediatrics and Genetics · USGeorgetown University · USUniversity of Pennsylvania · US

Funding

Regulation of NMDA Receptors in Excitotoxicity by Calpain and FYNR01NS045986 · NINDS · CHILDREN'S HOSP OF PHILADELPHIA · PI LYNCH, DAVID ROBINSON · 2003 to 2011
$2.9M
Regulation of NMDA Receptors in Excitotoxicity by Calpain and FYNR56NS045986 · NINDS · CHILDREN'S HOSP OF PHILADELPHIA · PI LYNCH, DAVID ROBINSON · 2007 to 2007
$413k
NINDS NIH HHS NS45986NINDS NIH HHS R01 NS045986NINDS NIH HHS R56 NS045986
6 · The paper itself

Abstract

In association with NMDA receptors (NMDARs), neuronal α7 nicotinic ACh receptors (nAChRs) have been implicated in neuronal plasticity as well as neurodevelopmental, neurological, and psychiatric disorders. However, the role of presynaptic NMDARs and their interaction with α7 nAChRs in these physiological and pathophysiological events remains unknown. Here we report that axonal α7 nAChRs modulate presynaptic NMDAR expression and structural plasticity of glutamatergic presynaptic boutons during early synaptic development. Chronic inactivation of α7 nAChRs markedly increased cell surface NMDAR expression as well as the number and size of glutamatergic axonal varicosities in cortical cultures. These boutons contained presynaptic NMDARs and α7 nAChRs, and recordings from outside-out pulled patches of enlarged presynaptic boutons identified functional NMDAR-mediated currents. Multiphoton imaging of presynaptic NMDAR-mediated calcium transients demonstrated significantly larger responses in these enlarged boutons, suggesting enhanced presynaptic NMDAR function that could lead to increased glutamate release. Moreover, whole-cell patch clamp showed a significant increase in synaptic charge mediated by NMDAR miniature EPSCs but no alteration in the frequency of AMPAR miniature EPSCs, suggesting the selective enhancement of postsynaptically silent synapses upon inactivation of α7 nAChRs. Taken together, these findings indicate that axonal α7 nAChRs modulate presynaptic NMDAR expression and presynaptic and postsynaptic maturation of glutamatergic synapses, and implicate presynaptic α7 nAChR/NMDAR interactions in synaptic development and plasticity.

Indexed as

alpha7 Nicotinic Acetylcholine ReceptorAnimalsAxonsCalcium SignalingCells, CulturedExcitatory Postsynaptic PotentialsMiniature Postsynaptic PotentialsNeuronal PlasticityNeuronsPatch-Clamp TechniquesPresynaptic TerminalsRatsReceptors, NicotinicReceptors, N-Methyl-D-Aspartatealpha7 Nicotinic Acetylcholine ReceptorChrna7 protein, ratReceptors, NicotinicReceptors, N-Methyl-D-Aspartate

Identifiers

PMID20817852
PMCPMC2944730
OpenAlexW2156319775

What OpenQuestion holds

Textmetadata
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.