Evidence map›Paper›PMID 24530419›Full record

ReviewEuropean journal of pharmacology2014

The therapeutic promise of positive allosteric modulation of nicotinic receptors.

Victor V Uteshev

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in European journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
6.3field-weighted citation impact, top 3% 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

55 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  4. Article
  5. Review
  6. Hidden complexity of α7 nicotinic acetylcholine receptor desensitization revealed by MD simulations and Markov state modeling.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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  10. Review
  11. Article
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  15. Review
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  19. Inhaled aerosolized nicotine suppresses the lung eosinophilic response to house dust mite allergen.American journal of physiology. Lung cellular and molecular physiology · 2020
    Article
  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

1 author at 1 institution in 1 country.

Victor V UteshevDepartment of Pharmacology and Neuroscience, University of North Texas Health Science Center, Fort Worth, TX 76107, USA. Electronic address: Victor.Uteshev@unthsc.edu.
University of North Texas · US

Funding

Responsiveness to nicotine of nucleus tractus solitarius neuronsR01DK082625 · NIDDK · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI UTESHEV, VICTOR V · 2009 to 2013
$1.7M
NIDDK NIH HHS DK082625NIDDK NIH HHS R01 DK082625
6 · The paper itself

Abstract

In the central nervous system, deficits in cholinergic neurotransmission correlate with decreased attention and cognitive impairment, while stimulation of neuronal nicotinic acetylcholine receptors improves attention, cognitive performance and neuronal resistance to injury as well as produces robust analgesic and anti-inflammatory effects. The rational basis for the therapeutic use of orthosteric agonists and positive allosteric modulators (PAMs) of nicotinic receptors arises from the finding that functional nicotinic receptors are ubiquitously expressed in neuronal and non-neuronal tissues including brain regions highly vulnerable to traumatic and ischemic types of injury (e.g., cortex and hippocampus). Moreover, functional nicotinic receptors do not vanish in age-, disease- and trauma-related neuropathologies, but their expression and/or activation levels decline in a subunit- and brain region-specific manner. Therefore, augmenting the endogenous cholinergic tone by nicotinic agents is possible and may offset neurological impairments associated with cholinergic hypofunction. Importantly, because neuronal damage elevates extracellular levels of choline (a selective agonist of α7 nicotinic acetylcholine receptors) near the site of injury, α7-PAM-based treatments may augment pathology-activated α7-dependent auto-therapies where and when they are most needed (i.e., in the penumbra, post-injury). Thus, nicotinic-PAM-based treatments are expected to augment the endogenous cholinergic tone in a spatially and temporally restricted manner creating the potential for differential efficacy and improved safety as compared to exogenous orthosteric nicotinic agonists that activate nicotinic receptors indiscriminately. In this review, I will summarize the existing trends in therapeutic applications of nicotinic PAMs.

Indexed as

AnalgesicsAnimalsAnti-Inflammatory AgentsCentral Nervous SystemDrug DesignHumansMolecular Targeted TherapyNeuroprotective AgentsNicotinic AgonistsNootropic AgentsReceptors, NicotinicSignal TransductionAnalgesicsAnti-Inflammatory AgentsNeuroprotective AgentsNicotinic AgonistsNootropic AgentsReceptors, Nicotinic1-(5-chloro-2,4-dimethoxyphenyl)-3-(5-methylisoxazol-3-yl)urea3-(2,4-dimethoxybenzylidene)-anabaseine)AnalgesiaCerebral ischemiaCholinecholine chloride (PubChem CID: 6209)epibatidine (PubChem CID: 854023)i.e., ABT-594 (PubChem CID: 3075702)i.e., DMXB-A (PubChem CID: 6438361)i.e., PNU-120596 (PubChem CID: 311434)Nicotinic acetylcholine receptorPNU-120596Positive allosteric modulator(R)-5-(2-azetidinylmethoxy)-2-chloropyridine

Identifiers

PMID24530419
PMCPMC3982318
OpenAlexW2042675067

What OpenQuestion holds

Textmetadata
LicenceTDM
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.