Evidence map›Paper›PMID 11274373›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2001

beta -Amyloid peptide blocks the response of alpha 7-containing nicotinic receptors on hippocampal neurons.

Q Liu, H Kawai, D K Berg

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed
–field-weighted citation impact
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

106 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Astrocyte-to-neuron HNature metabolism · 2025
    Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Sex-dependent cholinergic effects on amyloid pathology: A translational study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Significance of GABAInternational journal of molecular sciences · 2021
    Review
  18. Unbalanced Regulation of α7 nAChRs by Ly6h and NACHO Contributes to Neurotoxicity in Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  19. Article
  20. Article

46 more citing papers are in PubMed but not listed here.

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

3 authors.

Q LiuNeurobiology Section, Division of Biology, University of California at San Diego, La Jolla, CA 92093-0357, USA.
H Kawai
D K Berg

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
NINDS NIH HHS NS12601NINDS NIH HHS NS35469NINDS NIH HHS R01 NS012601
6 · The paper itself

Abstract

Alzheimer's disease produces a devastating decline in mental function, with profound effects on learning and memory. Early consequences of the disease include the specific loss of cholinergic neurons in brain, diminished cholinergic signaling, and the accumulation of beta-amyloid peptide in neuritic plaques. Of the nicotinic acetylcholine receptors at risk, the most critical may be those containing the alpha7 gene product (alpha7-nAChRs), because they are widespread, have a high relative permeability to calcium, and regulate numerous cellular events in the nervous system. With the use of whole-cell patch-clamp recording we show here that nanomolar concentrations of beta-amyloid peptides specifically and reversibly block alpha7-nAChRs on rat hippocampal neurons in culture. The block is noncompetitive, voltage-independent, and use-independent and is mediated through the N-terminal extracellular domain of the receptor. It does not appear to require either calcium influx or G protein activation. beta-Amyloid blockade is likely to be a common feature of alpha7-nAChRs because it applies to the receptors at both somato-dendritic and presynaptic locations on rat hippocampal neurons and extends to homologous receptors on chick ciliary ganglion neurons as well. Because alpha7-nAChRs in the central nervous system are thought to have numerous functions and recently have been implicated in learning and memory, impaired receptor function in this case may contribute to cognitive deficits associated with Alzheimer's disease.

Indexed as

Amyloid beta-PeptidesAnimalsCells, CulturedHippocampusNeuronsPeptide FragmentsRatsRats, Sprague-DawleyReceptors, NicotinicReceptors, SerotoninReceptors, Serotonin, 5-HT3Recombinant Fusion ProteinsAmyloid beta-Peptidesamyloid beta-protein (1-40)amyloid beta-protein (1-42)Peptide FragmentsReceptors, NicotinicReceptors, SerotoninReceptors, Serotonin, 5-HT3Recombinant Fusion Proteins

Identifiers

PMID11274373
PMCPMC31903

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.