Evidence map›Paper›PMID 24381273›Full record

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

Presynaptic α7 nicotinic acetylcholine receptors enhance hippocampal mossy fiber glutamatergic transmission via PKA activation.

Qing Cheng, Jerrel L Yakel

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 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

38 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Article
  3. Differential Regulation of Prelimbic and Thalamic Transmission to the Basolateral Amygdala by Acetylcholine Receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. 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
  9. Article
  10. Article
  11. Article
  12. Endogenous Cholinergic Signaling Modulates Sound-Evoked Responses of the Medial Nucleus of the Trapezoid Body.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  13. CaCells · 2020
    Review
  14. Review
  15. Article
  16. Article
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  20. Review
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

2 authors at 2 institutions in 1 country.

Qing ChengLaboratory of Neurobiology, National Institute of Environmental Health Sciences/National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina 27709.
Jerrel L Yakel
National Institute of Environmental Health Sciences · USNational Institutes of Health · US

Funding

Modulation Of Neuronal Channels and Receptors in the BrainZIAES090089 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI YAKEL, JERREL L · 2009 to 2025
$42.2M
Intramural NIH HHS
6 · The paper itself

Abstract

Nicotinic acetylcholine receptors (nAChRs) are expressed widely in the CNS, and mediate both synaptic and perisynaptic activities of endogenous cholinergic inputs and pharmacological actions of exogenous compounds (e.g., nicotine and choline). Behavioral studies indicate that nicotine improves such cognitive functions as learning and memory. However, the mechanism of nicotine's action on cognitive function remains elusive. We performed patch-clamp recordings from hippocampal CA3 pyramidal neurons to determine the effect of nicotine on mossy fiber glutamatergic synaptic transmission. We found that nicotine in combination with NS1738, an α7 nAChR-positive allosteric modulator, strongly potentiated the amplitude of evoked EPSCs (eEPSCs), and reduced the EPSC paired-pulse ratio. The action of nicotine and NS1738 was mimicked by PNU-282987 (an α7 nAChR agonist), and was absent in α7 nAChR knock-out mice. These data indicate that activation of α7 nAChRs was both necessary and sufficient to enhance the amplitude of eEPSCs. BAPTA applied postsynaptically failed to block the action of nicotine and NS1738, suggesting again a presynaptic action of the α7 nAChRs. We also observed α7 nAChR-mediated calcium rises at mossy fiber giant terminals, indicating the presence of functional α7 nAChRs at presynaptic terminals. Furthermore, the addition of PNU-282987 enhanced action potential-dependent calcium transient at these terminals. Last, the potentiating effect of PNU-282987 on eEPSCs was abolished by inhibition of protein kinase A (PKA). Our findings indicate that activation of α7 nAChRs at presynaptic sites, via a mechanism involving PKA, plays a critical role in enhancing synaptic efficiency of hippocampal mossy fiber transmission.

Indexed as

alpha7 Nicotinic Acetylcholine ReceptorAnimalsBenzamidesBridged Bicyclo CompoundsCyclic AMP-Dependent Protein KinasesEnzyme ActivationFemaleGlutamic AcidMaleMiceMice, Inbred C57BLMice, KnockoutMossy Fibers, HippocampalPhenylurea CompoundsPresynaptic TerminalsSynaptic Transmission1-(5-chloro-2-hydroxyphenyl)-3-(2-chloro-5-trifluoromethylphenyl)ureaalpha7 Nicotinic Acetylcholine ReceptorBenzamidesBridged Bicyclo CompoundsCyclic AMP-Dependent Protein KinasesGlutamic AcidPhenylurea CompoundsPNU-282987

Identifiers

PMID24381273
PMCPMC3866480
OpenAlexW2071231521

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.