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Identification of nicotinic acetylcholine receptor subunit expression in early avian embryos
Author(s) -
Haroon Zoha,
Stathos Joseph,
Higgins Daniel,
Olley John T.,
Brauer Philip R.,
Reedy Mark V.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.962.3
Subject(s) - nicotine , nicotinic agonist , embryo , nicotinic acetylcholine receptor , acetylcholine receptor , embryogenesis , protein subunit , biology , receptor , embryonic stem cell , andrology , pharmacology , microbiology and biotechnology , medicine , genetics , neuroscience , gene
Most previous studies on nicotine used relatively high concentrations of nicotine, administered later in development. Using chick embryos as our model system, we have found a single low dose of nicotine (100 nM) administered during early development significantly retarded embryo growth, reduced heart rate, and increased the incidence of defects four days later. It is often assumed that nicotine's teratogenic effects are mediated by nicotinic acetylcholine receptors (nAChRs), whose expression at very early stages of embryonic development has not been thoroughly investigated. The objective was to identify which nAChR subunits are expressed during early avian embryogenesis. We performed RT‐PCR expression analysis for eleven nAChR subunits, including alpha1‐alpha7, alpha9, alpha10, beta3, and beta4, at 24‐, 48‐, 72‐, and 96‐hrs of development. Surprisingly, we find nAChR expression is widespread during early development, which suggests the teratogenic effects of nicotine were mediated by the early activation of nAChRs. Nebraska NIH‐INBRE Program; Nebraska Health and Human Services (LB595); Ferlic Undergraduate Summer Research Program, Creighton University College of Arts and SciencesGrant Funding Source : none current