Document Detail


Determinants of zinc potentiation on the alpha4 subunit of neuronal nicotinic receptors.
MedLine Citation:
PMID:  16189299     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We have shown previously that the function of neuronal nicotinic acetylcholine receptors can be modulated by zinc. This modulation varies from potentiation to inhibition, depending on receptor subunit composition and zinc concentration, with the alpha4beta2 and alpha4beta4 receptors displaying the most dramatic potentiation. In this study, we used site-directed mutagenesis to identify glutamate 59 and histidine 162 on the rat alpha4 subunit as potential mediators of zinc potentiation. By modeling the extracellular domain of the receptor pentamer, we locate these residues to two subunit-subunit interfaces that alternate with the two acetylcholine-binding interfaces. Substitution of a cysteine at either position allows additional reduction of zinc potentiation upon treatment with the methanethiosulfonate reagents N-biotinoylaminoethyl methanethiosulfonate (MTSEA-biotin) and [2-(trimethylammonium)ethyl] methanethiosulfonate. Mutagenesis and methanethiosulfonate treatment are most effective at position 162, and the presence of zinc hinders the reaction of MTSEA-biotin with the substituted cysteine at this position, suggesting that alpha4His162 participates in forming a coordination site for zinc. Mutagenesis and methanethiosulfonate treatment are less effective at position 59, suggesting that whereas alpha4Glu59 may be near the zinc coordination site, it may not be participating in coordination of the zinc ion. It is noteworthy that the position of alpha4Glu59 within the neuronal nAChR is identical to that of a residue that lines the benzodiazepine-binding site on GABA(A) receptors. We suggest that the zinc potentiation sites on neuronal nAChRs are structurally and functionally similar to the benzodiazepine-binding sites on GABA(A) receptors.
Authors:
Bernard Hsiao; Karla B Mihalak; Sarah E Repicky; Drew Everhart; Ana H Mederos; Arun Malhotra; Charles W Luetje
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2005-09-27
Journal Detail:
Title:  Molecular pharmacology     Volume:  69     ISSN:  0026-895X     ISO Abbreviation:  Mol. Pharmacol.     Publication Date:  2006 Jan 
Date Detail:
Created Date:  2005-12-29     Completed Date:  2006-02-07     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0035623     Medline TA:  Mol Pharmacol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  27-36     Citation Subset:  IM    
Affiliation:
Department of Molecular and Cellular Pharmacology, Miller School of Medicine, University of Miami, Miami, FL 33101, USA.
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MeSH Terms
Descriptor/Qualifier:
Amino Acid Sequence
Animals
Binding Sites
Calcium / metabolism
Ion Channel Gating
Molecular Sequence Data
Neurons / drug effects*,  metabolism
Receptors, Nicotinic / drug effects*,  metabolism,  physiology
Sequence Homology, Amino Acid
Xenopus laevis
Zinc / pharmacology*
Grant Support
ID/Acronym/Agency:
DA08102/DA/NIDA NIH HHS; GM069972/GM/NIGMS NIH HHS; MH66038/MH/NIMH NIH HHS; T32 HL07188/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Receptors, Nicotinic; 7440-66-6/Zinc; 7440-70-2/Calcium

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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