Evidence map›Paper›PMID 25002271›Full record

ArticleMolecular pharmacology2014

The novel α7β2-nicotinic acetylcholine receptor subtype is expressed in mouse and human basal forebrain: biochemical and pharmacological characterization.

Milena Moretti, Michele Zoli, Andrew A George, Ronald J Lukas, Francesco Pistillo, Uwe Maskos, Paul Whiteaker, Cecilia Gotti

Abstract read
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In one paragraph

Article in Molecular pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
–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

46 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. The cellular model for Alzheimer's disease research: PC12 cells.Frontiers in molecular neuroscience · 2022
    Pooled it
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  6. Analogs of α-conotoxin PnIC selectively inhibit α7β2- over α7-only subtype nicotinic acetylcholine receptors via a novel allosteric mechanism.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
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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

8 authors.

Milena MorettiCNR Institute of Neuroscience, Biometra University of Milan, Milan, Italy (M.M., F.P., C.G.); Section of Physiology and Neurosciences, Department of Biomedical, Metabolic, and Neural Sciences, University of Modena and Reggio Emilia, Modena, Italy (M.Z.); Division of Neurobiology, Barrow Neurologic Institute, Phoenix, Arizona (A.A.G., R.J.L., P.W.); and Centre National de la Recherche Scientifique, Unité Neurobiologie Intégrative des Systèmes Cholinergiques, Institut Pasteur, Paris, France (U.M.).
Michele ZoliCNR Institute of Neuroscience, Biometra University of Milan, Milan, Italy (M.M., F.P., C.G.); Section of Physiology and Neurosciences, Department of Biomedical, Metabolic, and Neural Sciences, University of Modena and Reggio Emilia, Modena, Italy (M.Z.); Division of Neurobiology, Barrow Neurologic Institute, Phoenix, Arizona (A.A.G., R.J.L., P.W.); and Centre National de la Recherche Scientifique, Unité Neurobiologie Intégrative des Systèmes Cholinergiques, Institut Pasteur, Paris, France (U.M.).
Andrew A GeorgeCNR Institute of Neuroscience, Biometra University of Milan, Milan, Italy (M.M., F.P., C.G.); Section of Physiology and Neurosciences, Department of Biomedical, Metabolic, and Neural Sciences, University of Modena and Reggio Emilia, Modena, Italy (M.Z.); Division of Neurobiology, Barrow Neurologic Institute, Phoenix, Arizona (A.A.G., R.J.L., P.W.); and Centre National de la Recherche Scientifique, Unité Neurobiologie Intégrative des Systèmes Cholinergiques, Institut Pasteur, Paris, France (U.M.).
Ronald J LukasCNR Institute of Neuroscience, Biometra University of Milan, Milan, Italy (M.M., F.P., C.G.); Section of Physiology and Neurosciences, Department of Biomedical, Metabolic, and Neural Sciences, University of Modena and Reggio Emilia, Modena, Italy (M.Z.); Division of Neurobiology, Barrow Neurologic Institute, Phoenix, Arizona (A.A.G., R.J.L., P.W.); and Centre National de la Recherche Scientifique, Unité Neurobiologie Intégrative des Systèmes Cholinergiques, Institut Pasteur, Paris, France (U.M.).
Francesco PistilloCNR Institute of Neuroscience, Biometra University of Milan, Milan, Italy (M.M., F.P., C.G.); Section of Physiology and Neurosciences, Department of Biomedical, Metabolic, and Neural Sciences, University of Modena and Reggio Emilia, Modena, Italy (M.Z.); Division of Neurobiology, Barrow Neurologic Institute, Phoenix, Arizona (A.A.G., R.J.L., P.W.); and Centre National de la Recherche Scientifique, Unité Neurobiologie Intégrative des Systèmes Cholinergiques, Institut Pasteur, Paris, France (U.M.).
Uwe MaskosCNR Institute of Neuroscience, Biometra University of Milan, Milan, Italy (M.M., F.P., C.G.); Section of Physiology and Neurosciences, Department of Biomedical, Metabolic, and Neural Sciences, University of Modena and Reggio Emilia, Modena, Italy (M.Z.); Division of Neurobiology, Barrow Neurologic Institute, Phoenix, Arizona (A.A.G., R.J.L., P.W.); and Centre National de la Recherche Scientifique, Unité Neurobiologie Intégrative des Systèmes Cholinergiques, Institut Pasteur, Paris, France (U.M.).
Paul WhiteakerCNR Institute of Neuroscience, Biometra University of Milan, Milan, Italy (M.M., F.P., C.G.); Section of Physiology and Neurosciences, Department of Biomedical, Metabolic, and Neural Sciences, University of Modena and Reggio Emilia, Modena, Italy (M.Z.); Division of Neurobiology, Barrow Neurologic Institute, Phoenix, Arizona (A.A.G., R.J.L., P.W.); and Centre National de la Recherche Scientifique, Unité Neurobiologie Intégrative des Systèmes Cholinergiques, Institut Pasteur, Paris, France (U.M.) c.gotti@in.cnr paul.whiteaker@dignityhealth.org.
Cecilia GottiCNR Institute of Neuroscience, Biometra University of Milan, Milan, Italy (M.M., F.P., C.G.); Section of Physiology and Neurosciences, Department of Biomedical, Metabolic, and Neural Sciences, University of Modena and Reggio Emilia, Modena, Italy (M.Z.); Division of Neurobiology, Barrow Neurologic Institute, Phoenix, Arizona (A.A.G., R.J.L., P.W.); and Centre National de la Recherche Scientifique, Unité Neurobiologie Intégrative des Systèmes Cholinergiques, Institut Pasteur, Paris, France (U.M.) c.gotti@in.cnr paul.whiteaker@dignityhealth.org.

Funding

Construction and Expression of Concatemeric alpha6beta2* Nicotinic Acetycholine RR21DA026627 · NIDA · ST. JOSEPH'S HOSPITAL AND MEDICAL CENTER · PI WHITEAKER, PAUL · 2009 to 2010
$407k
Medical Research Council G0400074Medical Research Council G0502157Medical Research Council G0900652Medical Research Council G1100540Medical Research Council MR/L016451/1NIDA NIH HHS R21 DA026627NIDA NIH HHS R21-DA026627
6 · The paper itself

Abstract

We examined α7β2-nicotinic acetylcholine receptor (α7β2-nAChR) expression in mammalian brain and compared pharmacological profiles of homomeric α7-nAChRs and α7β2-nAChRs. α-Bungarotoxin affinity purification or immunoprecipitation with anti-α7 subunit antibodies (Abs) was used to isolate nAChRs containing α7 subunits from mouse or human brain samples. α7β2-nAChRs were detected in forebrain, but not other tested regions, from both species, based on Western blot analysis of isolates using β2 subunit-specific Abs. Ab specificity was confirmed in control studies using subunit-null mutant mice or cell lines heterologously expressing specific human nAChR subtypes and subunits. Functional expression in Xenopus oocytes of concatenated pentameric (α7)5-, (α7)4(β2)1-, and (α7)3(β2)2-nAChRs was confirmed using two-electrode voltage clamp recording of responses to nicotinic ligands. Importantly, pharmacological profiles were indistinguishable for concatenated (α7)5-nAChRs or for homomeric α7-nAChRs constituted from unlinked α7 subunits. Pharmacological profiles were similar for (α7)5-, (α7)4(β2)1-, and (α7)3(β2)2-nAChRs except for diminished efficacy of nicotine (normalized to acetylcholine efficacy) at α7β2- versus α7-nAChRs. This study represents the first direct confirmation of α7β2-nAChR expression in human and mouse forebrain, supporting previous mouse studies that suggested relevance of α7β2-nAChRs in Alzheimer disease etiopathogenesis. These data also indicate that α7β2-nAChR subunit isoforms with different α7/β2 subunit ratios have similar pharmacological profiles to each other and to α7 homopentameric nAChRs. This supports the hypothesis that α7β2-nAChR agonist activation predominantly or entirely reflects binding to α7/α7 subunit interface sites.

Indexed as

alpha7 Nicotinic Acetylcholine ReceptorAnimalsBinding SitesBridged Bicyclo Compounds, HeterocyclicBungarotoxinsCerebellumFemaleHippocampusHumansMaleMiceMice, Inbred C57BLMice, KnockoutNicotinic AgonistsNicotinic AntagonistsOocytesalpha7 Nicotinic Acetylcholine ReceptorBridged Bicyclo Compounds, HeterocyclicBungarotoxinsepibatidineNicotinic AgonistsNicotinic AntagonistsProtein SubunitsPyridinesReceptors, Nicotinic

Identifiers

PMID25002271
PMCPMC4152907

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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.