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Research ArticleArticle

Potentiation of α7-Containing Nicotinic Acetylcholine Receptors by Select Albumins

William G. Conroy, Qing-Song Liu, Qiang Nai, Joseph F. Margiotta and Darwin K. Berg
Molecular Pharmacology February 2003, 63 (2) 419-428; DOI: https://doi.org/10.1124/mol.63.2.419
William G. Conroy
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Qing-Song Liu
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Qiang Nai
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Joseph F. Margiotta
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Darwin K. Berg
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Abstract

Nicotinic receptors containing α7 subunits are ligand-gated ion channels widely distributed in the nervous system; they influence a diverse array of events because of their high relative calcium permeability. We show here that nicotine-induced whole-cell responses generated by such receptors can be dramatically potentiated in a rapidly reversible manner by some but not all albumins. The potentiation involves increases both in potency and efficacy with no obvious differences in rise and fall times of the response. The potentiation is not reduced by removing absorbed components; it is abolished by proteolysis, suggesting that the albumin protein backbone is essential. The fact that some albumins are ineffective indicates that minor differences in amino acid sequence may be critical. Experiments with open channel blockers indicate that the potentiation involves increased responses from active receptors rather than recruitment of receptors from a previously silent pool. Single channel recordings reveal that the potentiation correlates with increased single channel opening probability, reflected in increased frequency of channel opening and increased mean channel open time. The potentiation can be exploited to overcome blockade by noncompetitive inhibitors such as β-amyloid peptide. The results raise the possibility that endogenous compounds use the site to modulate receptor function in vivo, and suggest that the receptors may represent useful targets for therapeutic intervention in cases where they have been implicated in neuropathologies such as Alzheimer's disease.

Footnotes

  • This study was supported by Tobacco-Related Disease Research Program Grants 9RT-0058 (to W.G.C.) and 9RT-0221, and by National Institutes of Health Grants NS12601, NS35469 (to D.K.B.), and NS24417 (to J.F.M.). Q.-S.L. is an American Heart Association Postdoctoral Fellow.

  • W.G.C. and Q.-S.L. contributed equally to this work.

  • Abbreviations:
    nAChR
    nicotinic acetylcholine receptor
    NMDA
    N-methyl-d-aspartate
    PACAP
    pituitary adenylyl cyclase-activating protein
    E
    embryonic day
    αBgt
    α-bungarotoxin
    RS
    standard recording solution
    BSA
    bovine serum albumin
    Aβ
    β-amyloid peptide1–42
    BAPTA
    1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid
    • Received September 6, 2002.
    • Accepted October 21, 2002.
  • The American Society for Pharmacology and Experimental Therapeutics
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Molecular Pharmacology: 63 (2)
Molecular Pharmacology
Vol. 63, Issue 2
1 Feb 2003
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Research ArticleArticle

Potentiation of α7-Containing Nicotinic Acetylcholine Receptors by Select Albumins

William G. Conroy, Qing-Song Liu, Qiang Nai, Joseph F. Margiotta and Darwin K. Berg
Molecular Pharmacology February 1, 2003, 63 (2) 419-428; DOI: https://doi.org/10.1124/mol.63.2.419

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Research ArticleArticle

Potentiation of α7-Containing Nicotinic Acetylcholine Receptors by Select Albumins

William G. Conroy, Qing-Song Liu, Qiang Nai, Joseph F. Margiotta and Darwin K. Berg
Molecular Pharmacology February 1, 2003, 63 (2) 419-428; DOI: https://doi.org/10.1124/mol.63.2.419
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