Evidence map›Paper›PMID 24501347›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014

A novel mechanism for nicotinic potentiation of glutamatergic synapses.

Andrew W Halff, David Gómez-Varela, Danielle John, Darwin K Berg

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

35 citing papers in PubMed, 57 citations in OpenAlex.

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  13. Nicotinic acetylcholine receptor subunit αJournal of neurophysiology · 2019
    Article
  14. Article
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  19. Article
  20. Memory replay in balanced recurrent networks.PLoS computational biology · 2017
    Article
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

4 authors at 3 institutions in 2 countries.

Andrew W HalffNeurobiology Section, Division of Biological Sciences, University of California-San Diego, La Jolla, California 92093, and Max Planck Institute of Experimental Medicine, 37075 Göttingen, Germany.
David Gómez-Varela
Danielle John
Darwin K Berg
University of California San Diego · USMax Planck Institute of Experimental Medicine · DEMax Planck Society · DE

Funding

Signal Transduction at Neuronal Nicotinic SynapsesR01NS012601 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BERG, DARWIN K · 1985 to 2016
$5.3M
Nicotinic Control of Non-Nicotinic Synapses in the HippocampusR01NS035469 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BERG, DARWIN K · 1996 to 2013
$4.8M
Nicotinic Mechanisms Driving Glutamate Synaptogenesis and Spine FormationF31NS068016 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HALFF, ANDREW WILLIAM · 2010 to 2012
$95k
NINDS NIH HHS F31 NS068016NINDS NIH HHS NS012601NINDS NIH HHS NS035469NINDS NIH HHS NS068016NINDS NIH HHS R01 NS012601NINDS NIH HHS R01 NS035469
6 · The paper itself

Abstract

Selective strengthening of specific glutamatergic synapses in the mammalian hippocampus is critical for encoding new memories. This is most commonly achieved by input-specific Hebbian-type plasticity involving glutamate-dependent coincident presynaptic and postsynaptic depolarization. Our results demonstrate a novel mechanism by which nicotinic signaling, independently of coincident fast glutamatergic transmission, increases synaptic strength in the hippocampus. Electrophysiological recordings from rat hippocampal neurons in culture revealed that 1-3 h of exposure to 1 μm nicotine, even with action potentials being blocked, produced increases in both the frequency and amplitude of miniature EPSCs. Possible mechanisms were analyzed both in mouse organotypic slice culture and in rat cell culture by inducing the cells to express super-ecliptic pHluorin-tagged GluA1-containing AMPA receptors, which fluoresce only on the cell surface. Pharmacological and genetic manipulation of the cells, in combination with fluorescence-recovery-after-photobleaching experiments, revealed that nicotine, acting through α7-containing nicotinic acetylcholine receptors on the postsynaptic neuron, induces the stabilization and accumulation of GluA1-containing AMPA receptors on dendritic spines. The process relies on intracellular calcium signaling, PDZ [postsynaptic density-95 (PSD-95)/Discs large (Dlg)/zona occludens-1 (ZO-1)] interactions with members of the PSD-95 family, and lateral diffusion of the GluA1 receptors on the cell surface. These findings define a new avenue by which nicotinic signaling modulates synaptic mechanisms thought to subserve learning and memory.

Indexed as

AnimalsAnimals, NewbornExcitatory Postsynaptic PotentialsFemaleGlutamic AcidHippocampusMaleMiceMice, Inbred C57BLNicotineOrgan Culture TechniquesRatsRats, Sprague-DawleyReceptors, AMPASynapsesGlutamic AcidNicotineReceptors, AMPAFRAPGluA1hippocampusnAChRnicotineplasticity

Identifiers

PMID24501347
PMCPMC3913862
OpenAlexW1972708666

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.