Evidence map›Paper›PMID 19457164›Full record

ArticleJournal of neurochemistry2009

Defining pre-synaptic nicotinic receptors regulated by beta amyloid in mouse cortex and hippocampus with receptor null mutants.

Tejal K Mehta, John J Dougherty, Jianlin Wu, Catherine H Choi, Ghous M Khan, Robert A Nichols

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neurochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

15 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
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  5. Review
  6. Article
  7. Review
  8. Regulation of presynaptic Ca2+, synaptic plasticity and contextual fear conditioning by a N-terminal β-amyloid fragment.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  9. Article
  10. Article
  11. Article
  12. Amyloid oligomer neurotoxicity, calcium dysregulation, and lipid rafts.International journal of Alzheimer's disease · 2011
    Article
  13. Article
  14. Review
  15. 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

6 authors at 2 institutions in 1 country.

Tejal K MehtaDepartment of Pharmacology & Physiology, Drexel University College of Medicine, Philadelphia, PA, USA.
John J Dougherty
Jianlin Wu
Catherine H Choi
Ghous M Khan
Robert A Nichols
Drexel University · USUniversity of Hawaiʻi at Mānoa · US

Funding

Beta Amyloid and Presynaptic Nicotinic ReceptorsR01AG021586 · NIA · UNIVERSITY OF HAWAII AT MANOA · PI NICHOLS, ROBERT ALAN · 2004 to 2007
$887k
NIA NIH HHS AG21586NIA NIH HHS R01 AG021586
6 · The paper itself

Abstract

Disruption of neuronal signaling by soluble beta-amyloid has been implicated in deficits in short-term recall in the early stages of Alzheimer's disease. One potential target for beta-amyloid is the synapse, with evidence for differential interaction with both pre- and post-synaptic elements. Our previous work revealed an agonist-like action of soluble beta-amyloid (pM to nM) on isolated pre-synaptic terminals to increase [Ca(2+)]i, with apparent involvement of pre-synaptic nicotinic receptors. To directly establish the role of nicotinic receptors in pre-synaptic Ca(2+) regulation, we investigated the pre-synaptic action of beta-amyloid on terminals isolated from mice harboring either beta2 or alpha7 nicotinic receptor null mutants (knockouts). Average pre-synaptic responses to beta-amyloid in hippocampal terminals of alpha7 knockout mice were unchanged, whereas responses in hippocampal terminals from beta2 knockout mice were strongly attenuated. In contrast, pre-synaptic responses to soluble beta-amyloid were strongly attenuated in cortical terminals from alpha7 knockout mice but were moderately attenuated in cortical terminals from beta2 knockout mice. The latter responses, having distinct kinetics, were completely blocked by alpha-bungarotoxin. The use of receptor null mutants thus permitted direct demonstration of the involvement of specific nicotinic receptors in pre-synaptic Ca(2+) regulation by soluble beta-amyloid, and also indicated differential neuromodulation by beta-amyloid of synapses in hippocampus and cortex.

Indexed as

alpha7 Nicotinic Acetylcholine ReceptorAmyloid beta-PeptidesAnimalsBungarotoxinsCalciumCerebral CortexHippocampusMiceMice, Inbred C57BLMice, KnockoutNicotineNicotinic AgonistsPeptide FragmentsReceptors, NicotinicSynaptosomesalpha7 Nicotinic Acetylcholine ReceptorAmyloid beta-Peptidesamyloid beta-protein (1-42)BungarotoxinsCalciumChrna7 protein, mouseNicotineNicotinic AgonistsPeptide FragmentsReceptors, Nicotinic

Identifiers

PMID19457164
PMCPMC3979963
OpenAlexW1963529280

What OpenQuestion holds

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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.